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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Lyz2tm1(cre)Ifo
targeted mutation 1, Irmgard Forster
MGI:1934631
Summary 160 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Lyz2tm1(cre)Ifo/Lyz2+ involves: 129P2/OlaHsd * C57BL/6 MGI:5014089
cn2
Apba3tm1.1Ski/Apba3tm1.1Ski
Lyz2tm1(cre)Ifo/Lyz2+
B6.129-Apba3tm1.1Ski Lyz2tm1(cre)Ifo MGI:5293148
cn3
Elavl1tm1.1Bndr/Elavl1tm1.1Bndr
Lyz2tm1(cre)Ifo/Lyz2+
B6.129-Elavl1tm1.1Bndr MGI:5316084
cn4
Elavl1tm1.1Dkon/Elavl1tm1.1Dkon
Lyz2tm1(cre)Ifo/Lyz2+
B6.129P2-Elavl1tm1.1Dkon Lyz2tm1(cre)Ifo MGI:5429343
cn5
Nr3c1tm2Gsc/Nr3c1tm2Gsc
Lyz2tm1(cre)Ifo/Lyz2+
B6.129P2-Lyz2tm1(cre)Ifo Nr3c1tm2Gsc MGI:3817871
cn6
Myd88tm1Hlz/Myd88tm1Hlz
Lyz2tm1(cre)Ifo/Lyz2+
B6.129P2-Myd88tm1Hlz Lyz2tm1(cre)Ifo MGI:5442780
cn7
Thbdtm1.1Hlwu/Thbdtm1.1Hlwu
Lyz2tm1(cre)Ifo/Lyz2+
B6.129-Thbdtm1.1Hlwu Lyz2tm1(cre)Ifo MGI:5445365
cn8
Arg1tm1Pmu/Arg1tm1Pmu
Lyz2tm1(cre)Ifo/?
B6.Cg-Arg1tm1Pmu Lyz2tm1(cre)Ifo MGI:3826860
cn9
Cd1d1tm1.1Aben/Cd1d1tm1.1Aben
Lyz2tm1(cre)Ifo/Lyz2+
B6.Cg-Cd1d1tm1.1Aben Lyz2tm1(cre)Ifo MGI:5318545
cn10
Cybbtm1.1Abk/Cybbtm1.1Abk
Lyz2tm1(cre)Ifo/?
B6.Cg-Lyz2tm1(cre)Ifo Cybbtm1.1Abk MGI:6192679
cn11
Naipctm1Kmma/Naipctm1Kmma
Lyz2tm1(cre)Ifo/Lyz2+
B6.Cg-Lyz2tm1(cre)Ifo Naipctm1Kmma MGI:5896660
cn12
Plekhf1tm1.1Caox/Plekhf1tm1.1Caox
Lyz2tm1(cre)Ifo/Lyz2+
B6.Cg-Plekhf1tm1.1Caox Lyz2tm1(cre)Ifo MGI:6360685
cn13
Mapk8tm1Rjd/Mapk8tm1Rjd
Mapk9tm2.1Rjd/Mapk9tm2.1Rjd
Lyz2tm1(cre)Ifo/Lyz2+
B6J.Cg-Lyz2tm1(cre)Ifo Mapk9tm2.1Rjd Mapk8tm1Rjd MGI:5882343
cn14
Nr3c1tm2Gsc/Nr3c1tm2Gsc
Lyz2tm1(cre)Ifo/Lyz2+
C.129P2-Lyz2tm1(cre)Ifo Nr3c1tm2Gsc MGI:4455049
cn15
Il1rntm1.1Cga/Il1rntm1.1Cga
Lyz2tm1(cre)Ifo/Lyz2+
D1.Cg-Il1rntm1.1Cga Lyz2tm1(cre)Ifo MGI:4819947
cn16
Hmox1tm1.1Gkl/Hmox1tm1.1Gkl
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * 129P2/OlaHsd * BALB/cJ * C57BL/6 MGI:3846105
cn17
Tnftm1.1Sned/Tnftm1.1Sned
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * 129P2/OlaHsd * C57BL/6 MGI:3527247
cn18
Lyz2tm1(cre)Ifo/Lyz2+
Pdcd10tm1Wami/Pdcd10tm1Wami
involves: 129 * 129P2/OlaHsd * C57BL/6 MGI:6158666
cn19
Cfptm2.1Song/Cfptm2.1Song
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * 129P2/OlaHsd * C57BL/6 * SJL MGI:4838306
cn20
Il1r1tm1Roml/Il1r1tm1Roml
Nlrp3tm1Hhf/Nlrp3+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:3850053
cn21
Nlrp3tm1Flv/Nlrp3tm1Hhf
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:3850059
cn22
Ptgestm1.1Gaf/Ptgestm1.1Gaf
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:5570434
cn23
Nlrp3tm1Hhf/Nlrp3+
Pycardtm1Flv/Pycardtm1Flv
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:3850058
cn24
Gt(ROSA)26Sortm1(CAG-CAMK2G*T287D,-EGFP)Whua/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:6093456
cn25
Mef2ctm1Jjs/Mef2ctm1Jjs
Mir223tm1Fcam/Mir223tm1Fcam
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:3811199
cn26
Socs3tm1Ayos/Socs3tm1Ayos
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 MGI:3051636
cn27
Rfx5tm1Ifo/Rfx5tm1.1Ifo
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6 * C.B-20 MGI:3844880
cn28
Vegfatm2Gne/Vegfatm2Gne
Lyz2tm1(cre)Ifo/Lyz2+
Tg(KRT14-cre)1Cgn/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5444295
cn29
Pcyt1atm1Irt/Pcyt1atm1Irt
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129 * C57BL/6J MGI:3027959
cn30
Adam17tm1Bbl/Adam17tm1Bbl
Lyz2tm1(cre)Ifo/0
involves: 129P2/OlaHsd MGI:3810470
cn31
Cflartm1.1Pope/Cflartm1.2Pope
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:4868712
cn32
Rb1cc1tm1.1Guan/Rb1cc1tm1.1Guan
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:6287982
cn33
P4hbtm1.1Geno/P4hbtm1.2Geno
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:5504638
cn34
Ltbrtm1Avt/Ltbrtm1Avt
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:4453320
cn35
Sqstm1tm2.1Jmos/Sqstm1tm2.1Jmos
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:5487464
cn36
Lyz2tm1(cre)Ifo/Lyz2tm1(cre)Ifo
Nrrostm1Wouy/Nrrostm1Wouy
involves: 129P2/OlaHsd MGI:6144087
cn37
Hmgb1tm1.1Ttg/Hmgb1tm1.1Ttg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:5563539
cn38
Stk11tm1Keis/Stk11tm1Keis
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:5470074
cn39
Syktm1.1Nns/Syktm1.1Nns
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:5314236
cn40
Engtm2.1Hma/Engtm2.1Hma
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:5775293
cn41
Becn1tm1Ebr/Becn1tm1Ebr
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd MGI:6287976
cn42
Ctnnb1tm2Kem/Ctnnb1+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:5581947
cn43
Hif1atm3Rsjo/Hif1atm3Rsjo
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:4418465
cn44
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ MGI:5581946
cn45
Hif1atm3Rsjo/Hif1atm3Rsjo
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:4418500
cn46
Gbatm1Clk/Gbatm1.1Clk
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:3699187
cn47
Gt(ROSA)26Sortm1(OVAL/fla,GFP)Vnce/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
Pycardtm1Vmd/Pycardtm1Vmd
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:6196858
cn48
Cdkn2btm1Wff/Cdkn2btm1Wff
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 MGI:4829853
cn49
Il12btm1Jm/Il12btm1Jm
Stat3tm2Aki/Stat3tm2Aki
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 MGI:3771395
cn50
Esr2tm1.1Pcn/Esr2tm1.1Pcn
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S2/SvPas MGI:5298874
cn51
Itgamtm1Myd/Itgamtm1Myd
Syktm1Tyb/Syktm1.2Tara
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:4415250
cn52
Itgb3tm1Hyn/Itgb3tm1.1Wlbcr
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:5688877
cn53
Syktm1Tyb/Syktm1.2Tara
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:4415249
cn54
Itgavtm2Hyn/Itgavtm2.1Hyn
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * FVB MGI:3759847
cn55
Kmt2atm1.1Erns/Kmt2atm1.1Erns
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3839885
cn56
Vhltm1Jae/Vhltm1Jae
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4418464
cn57
Ptentm1Hwu/Ptentm1Hwu
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4836609
cn58
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4441491
cn59
Mcl1tm1Ywh/Mcl1tm1Ywh
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:3801426
cn60
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441492
cn61
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441488
cn62
Rxratm1Krc/Rxratm1Krc
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4939884
cn63
Rac1tm1Djk/Rac1tm1.1Djk
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:2663670
cn64
Tfpitm1.1Rdsi/Tfpitm1.1Rdsi
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S6/SvEvTac * BALB/cJ * C57BL/6 MGI:4836842
cn65
Myo18atm1c(KOMP)Wtsi/Myo18atm1c(KOMP)Wtsi
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6N MGI:6360589
cn66
Esr1tm1.1Scma/Esr1tm1.1Scma
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 MGI:4430565
cn67
Zc3h12ctm2c(EUCOMM)Hmgu/Zc3h12ctm2c(EUCOMM)Hmgu
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6N MGI:6359746
cn68
Klf2tm2Ling/Klf2tm2Ling
Lyz2tm1(cre)Ifo/0
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:5829819
cn69
Nr3c1tm2.1Ljm/Nr3c1tm2.1Ljm
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:5803964
cn70
Klf4tm1Khk/Klf4tm1Khk
Lyz2tm1(cre)Ifo/0
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:5829820
cn71
Abca1tm1Jp/Abca1tm1Jp
Abcg1tm1Tall/Abcg1tm1Tall
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 MGI:5451017
cn72
Ptpn11tm1Ckq/Ptpn11+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:5295468
cn73
Nfat5tm1.1Itl/Nfat5tm1.1Itl
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6NTac * FVB/N MGI:5522641
cn74
Ptpmt1tm2.1Ckq/Ptpmt1tm2.1Ckq
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL MGI:5485994
cn75
Apoetm1Lmh/Apoetm1Lmh
Ldlrtm1Her/Ldlrtm1Her
Lrp1tm2Her/Lrp1tm2Her
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:4943551
cn76
Ldlrtm1Her/Ldlrtm1Her
Lrp1tm2Her/Lrp1tm2Her
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:4943737
cn77
Ldlrtm1Her/Ldlrtm1Her
Lrp1tm2Her/Lrp1tm2Her
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:4943738
cn78
Atg5tm1Myok/Atg5tm1Myok
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEv MGI:6287975
cn79
Hsp90b1tm1Zhli/Hsp90b1tm1.1Zhli
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEv MGI:3700816
cn80
Tnftm2.1Gkl/Tnf+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEv * 129S6/SvEvTac * C57BL/6J MGI:3629610
cn81
Chuktm1Lex/Chuktm1Lex
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEvBrd MGI:4457384
cn82
Ikbkbtm1Lex/Ikbkbtm1Lex
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEvBrd MGI:4457386
cn83
Kmt2atm1.1(Sh3gl1)Lcc/Kmt2a+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 MGI:5559577
cn84
Tnftm2.1Gkl/Tnftm2.1Gkl
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J MGI:3629596
cn85
Fpr2tm1.1Jimw/Fpr2tm1.1Jimw
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129X1/SvJ MGI:5503981
cn86
Ctnnb1tm1Mmt/Ctnnb1+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129X1/SvJ MGI:5581954
cn87
Ppargtm1.1Gonz/Ppargtm1.1Gonz
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:4939883
cn88
Il15ratm1Ama/Il15ratm2.1Ama
Lyz2tm1(cre)Ifo/0
Tg(Itgax-cre)1-1Reiz/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * CBA MGI:4417844
cn89
Il15ratm1Ama/Il15ratm2.1Ama
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J MGI:4417843
cn90
Il4ratm1Fbb/Il4ratm2Fbb
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * BALB/c MGI:3690928
cn91
Il4ratm2Fbb/Il4ratm2Fbb
Lyz2tm1(cre)Ifo/?
involves: 129P2/OlaHsd * BALB/c MGI:5301111
cn92
Il10ratm1.1Jack/Il10ratm1.1Jack
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * BALB/c * C57BL/6 MGI:4437328
cn93
Pmltm1(PML/RARA)Ley/Pml+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 MGI:5014088
cn94
Ifnb1tm2.1Lien/Ifnb1tm2.1Lien
Tyrc-2J/Tyrc-2J
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5007898
cn95
Junbtm3Wag/Junbtm3Wag
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3036221
cn96
Nfkbiatm1Kbp/Nfkbiatm1Kbp
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3579004
cn97
Ube2ntm1Aki/Ube2ntm1Aki
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3656028
cn98
Il10tm2Roer/Il10tm2Roer
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3696707
cn99
Inpp5dtm1Rav/Inpp5dtm1.1Rav
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3716739
cn100
Stat3tm2Aki/Stat3tm2Aki
Tlr4tm1Aki/Tlr4tm1Aki
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3771394
cn101
Stat3tm2Aki/Stat3tm2Aki
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3771396
cn102
Hfetm1Wsr/Hfetm1Wsr
Lyz2tm1(cre)Ifo/?
involves: 129P2/OlaHsd * C57BL/6 MGI:3775663
cn103
Bcl2tm1Irt/Bcl2tm1Irt
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3830961
cn104
Apoetm1Bres/Apoetm1Bres
Bcl2tm1Irt/Bcl2tm1Irt
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3830965
cn105
Nfatc1tm3Glm/Nfatc1tm3Glm
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3831755
cn106
Traf6tm1.1Mpa/Traf6tm1.1Mpa
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3837131
cn107
Socs3tm1Wsa/Socs3tm2Wsa
Lyz2tm1(cre)Ifo/?
involves: 129P2/OlaHsd * C57BL/6 MGI:4430241
cn108
Fosl2tm2Wag/Fosl2tm2Wag
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:4834995
cn109
Adora2btm1Msit/Adora2btm1Msit
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:4941888
cn110
Ccl2tm1.1Pame/Ccl2tm1.1Pame
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:4950283
cn111
Fostm7Wag/Fostm7Wag
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5142265
cn112
Idh1tm1Mak/Idh1tm1Mak
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5438278
cn113
Idh1tm2Mak/Idh1tm2Mak
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5438279
cn114
Lyz2tm1(cre)Ifo/Lyz2+
Nfkbiztm1.1Muta/Nfkbiztm1.1Muta
involves: 129P2/OlaHsd * C57BL/6 MGI:5501492
cn115
Tab2tm2.1Aki/Tab2tm2.1Aki
Tab3tm1Aki/Tab3tm1Aki
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5502700
cn116
Il6ratm1.1Jcbr/Il6ratm1.1Jcbr
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5550556
cn117
Map3k7tm1.1Gkl/Map3k7tm1.1Gkl
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5577060
cn118
Atg16l1tm2.1Mvlc/Atg16l1tm2.1Mvlc
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:5605967
cn119
Il1r1tm1Quan/Il1r1tm1Quan
Lyz2tm1(cre)Ifo/Lyz2tm1(cre)Ifo
involves: 129P2/OlaHsd * C57BL/6 MGI:5638893
cn120
Cxcr4tm2Yzo/Cxcr4tm2Yzo
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:6116482
cn121
Zfp36tm1.1Xen/Zfp36tm1.1Xen
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6N MGI:5441587
cn122
Atg7tm1Tchi/Atg7tm1Tchi
Lyz2tm1(cre)Ifo/Lyz2+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2 MGI:6287974
cn123
Ccr2tm1Mpa/Ccr2tm1Mpa
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5444292
cn124
Upf2tm1Btp/Upf2tm1Btp
Lyz2tm1(cre)Ifo/?
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3797493
cn125
Stat3tm2Aki/Stat3tm2Aki
Tnftm1Sek/Tnftm1Sek
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3771397
cn126
n-TUtca2tm2Mym/n-TUtca2tm2.1Mym
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3772771
cn127
Nfe2l2tm1Mym/Nfe2l2tm1Mym
n-TUtca2tm2Mym/n-TUtca2tm2.1Mym
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3772772
cn128
Adcy7tm1.1Pcst/Adcy7tm1.1Pcst
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:5470146
cn129
Clec7atm1.1Bpip/Clec7atm1.1Bpip
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:5529128
cn130
Gt(ROSA)26Sortm1(OVAL/fla,GFP)Vnce/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:6196856
cn131
Pycardtm1Ayaz/Pycardtm1Ayaz
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:5467385
cn132
Notch2tm2.1Ecan/Notch2tm2.1Ecan
Lyz2tm1(cre)Ifo/Lyz2tm1(cre)Ifo
involves: 129P2/OlaHsd * C57BL/6J MGI:6157647
cn133
Notch2tm2.1Ecan/Notch2tm2.1Ecan
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:6157644
cn134
Elavl1tm1.1Dkon/Elavl1tm1.1Dkon
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:5429344
cn135
Rnf146tm1.1Rtpl/Rnf146tm1.1Rtpl
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J MGI:6150897
cn136
Hmox1tm1.1Hes/Hmox1tm1.1Hes
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J * C57BL/6N MGI:5660648
cn137
Gt(ROSA)26Sortm1(OVAL/fla,GFP)Vnce/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
Nlrc4tm1Vmd/Nlrc4tm1Vmd
involves: 129P2/OlaHsd * C57BL/6J * C57BL/6NCrl MGI:6196855
cn138
Trim58tm2313.1Arte/Trim58tm2313.1Arte
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6N MGI:6363314
cn139
Lyz2tm1(cre)Ifo/Lyz2+
Pikfyvetm1b(EUCOMM)Hmgu/Pikfyvetm1b(EUCOMM)Hmgu
involves: 129P2/OlaHsd * C57BL/6N MGI:6156769
cn140
Cers6tm1Arte/Cers6tm1Arte
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6N MGI:5607428
cn141
Atg7tm1Tchi/Atg7tm1Tchi
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6NCrlj * CBA/JNCrlj MGI:6287973
cn142
Slc3a2tm1.1Yait/Slc3a2tm1.1Yait
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6NCrSlc MGI:5440716
cn143
Ltbrtm1.1Thhe/Ltbrtm1.1Thhe
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5318484
cn144
Atf3tm1.1Hai/Atf3tm1.1Hai
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * FVB/N MGI:5547961
cn145
Casp8tm1Wll/Casp8tm1.1Yuan
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129S1/Sv * 129X1/SvJ * MF1 MGI:3055111
cn146
Ikbkbtm2Mka/Ikbkbtm2Mka
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd MGI:4843279
cn147
Vegfatm2Gne/Vegfatm2Gne
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd MGI:4418463
cn148
Nlrp3tm2Hhf/Nlrp3+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3850048
cn149
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1b+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714154
cn150
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714153
cn151
Vegfatm2Gne/Vegfatm2Gne
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:4418501
cn152
Nlrp3tm1Hhf/Nlrp3+
Rag1tm1Mom/Rag1tm1Mom
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3850056
cn153
Nlrp3tm1Hhf/Nlrp3+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3850045
cn154
Stat1tm1Rds/Stat1tm1Rds
Stat3tm2Aki/Stat3tm2Aki
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3771398
cn155
Vegfatm2Gne/Vegfatm2Gne
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * FVB/N MGI:5444293
cn156
Fmnl1tm1.2Sdb/Fmnl1tm1.2Sdb
Lyz2tm1(cre)Ifo/Lyz2tm1(cre)Ifo
involves: C3H * C57BL/6 * FVB/N MGI:6119817
cn157
Rpl13atm1.1Mazu/Rpl13atm1.1Mazu
Lyz2tm1(cre)Ifo/Lyz2+
involves: C57BL/6 MGI:5502329
cn158
Il6ratm1.1Drew/Il6ratm1.1Drew
Lyz2tm1(cre)Ifo/Lyz2+
involves: C57BL/6 * C57BL/6N * SJL MGI:4456458
cn159
Map3k8tm1.1Gkl/Map3k8tm1.1Gkl
Lyz2tm1(cre)Ifo/Lyz2+
involves: C57BL/6 * FVB/N MGI:5476713
cx160
Rnf146tm1.1Rtpl/Rnf146tm1.1Rtpl
Sh3bp2tm1c(KOMP)Wtsi/Sh3bp2tm1c(KOMP)Wtsi
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6J * C57BL/6N MGI:6150899


Genotype
MGI:5014089
ht1
Allelic
Composition
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system

immune system




Genotype
MGI:5293148
cn2
Allelic
Composition
Apba3tm1.1Ski/Apba3tm1.1Ski
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.129-Apba3tm1.1Ski Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apba3tm1.1Ski mutation (0 available); any Apba3 mutation (2 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

immune system
• LPS-treated mice exhibit increased survival compared with similarly treated wild-type mice

homeostasis/metabolism




Genotype
MGI:5316084
cn3
Allelic
Composition
Elavl1tm1.1Bndr/Elavl1tm1.1Bndr
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.129-Elavl1tm1.1Bndr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Elavl1tm1.1Bndr mutation (0 available); any Elavl1 mutation (18 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• fewer capillaries per muscle fiber in gastrocnemius after induced hind limb ischemia
• reduced microvessel formation in sterile sponges implanted subdermally
• reduced VEGF and MMP-9 in sterile sponges implanted subdermally
• considerable attenuation of blood flow in the gastrocnemius after induced hind limb ischemia

cellular
• higher level of necrosis in the paws of the hind limb at 2 weeks after induced hind limb ischemia




Genotype
MGI:5429343
cn4
Allelic
Composition
Elavl1tm1.1Dkon/Elavl1tm1.1Dkon
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.129P2-Elavl1tm1.1Dkon Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Elavl1tm1.1Dkon mutation (0 available); any Elavl1 mutation (18 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in response to LPS treatment, mice exhibit increased lethality compared with control mice

immune system
N
• mice exhibit normal myelopoiesis
• enhanced in response to CCR2 signals
• DSS-treated mice exhibit enhanced progression and maintenance of inflammatory colitis and 2 of 19 mice develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• in response to LPS treatment
• in response to LPS treatment
• in response to LPS treatment
• in response to LPS treatment
• in response to LPS treatment, mice exhibit increased lethality and increased serum levels of TNF, IL6, IL1B and IL12 compared with control mice

neoplasm
• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
• in mice treated with DSS and DMH

digestive/alimentary system
• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice
• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• DSS-treated mice exhibit enhanced progression and maintenance of inflammatory colitis and 2 of 19 mice develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice

homeostasis/metabolism
• in response to LPS treatment
• in response to LPS treatment
• in response to LPS treatment
• in response to LPS treatment
• in response to LPS treatment, mice exhibit increased lethality compared with control mice
• 2 of 19 mice DSS-treated develop neoplastic transformation in the form of early and late stage colonic epithelial adenomas compared with control mice
• mice treated with DSS and DMH exhibit increased incidence, number and size of tumor, mostly adenocarcinomas, compared with control mice

cellular
• enhanced in response to CCR2 signals

hematopoietic system
• enhanced in response to CCR2 signals




Genotype
MGI:3817871
cn5
Allelic
Composition
Nr3c1tm2Gsc/Nr3c1tm2Gsc
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.129P2-Lyz2tm1(cre)Ifo Nr3c1tm2Gsc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Nr3c1tm2Gsc mutation (1 available); any Nr3c1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice exhibit normal susceptibility to MOG induced experimental autoimmune encephalomyelitis and response to treatment with dexamethasone




Genotype
MGI:5442780
cn6
Allelic
Composition
Myd88tm1Hlz/Myd88tm1Hlz
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.129P2-Myd88tm1Hlz Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Myd88tm1Hlz mutation (1 available); any Myd88 mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in a model of septic peritonitis
• in a model of septic peritonitis
• in a model of septic peritonitis
• in a CASP model of septic peritonitis, mice exhibit reduced circulating CXCL1 compared with control mice
• in response to septic peritonitis, the peritoneal lavage fluid contains less CXCL10 compared with control mice
• in a model of septic peritonitis, mice exhibit aggravated liver injury compared with control mice

immune system
N
• mice exhibit normal expression of cytokines and neutrophil accumulation in inflammatory models
• in a model of septic peritonitis
• in a CASP model of septic peritonitis, mice exhibit reduced circulating CXCL1 compared with control mice
• in response to septic peritonitis, the peritoneal lavage fluid contains less CXCL10 compared with control mice




Genotype
MGI:5445365
cn7
Allelic
Composition
Thbdtm1.1Hlwu/Thbdtm1.1Hlwu
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.129-Thbdtm1.1Hlwu Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Thbdtm1.1Hlwu mutation (0 available); any Thbd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following cecal ligation and puncture

immune system
• in mice infected with K. pneumonia or following cecal ligation and puncture
• however, response to S. aureus is normal
• in mice infected with K. pneumonia or following cecal ligation and puncture
• in peritoneal macrophages from mice stimulated with LPS or K. pneumonia
• however, response to LTA and S. aureus is normal
• mice infected with K. pneumonia exhibit improved survival, decreased circulating levels of IL6 and TNFalpha, decreased bacterial dissemination and increased neutrophil infiltration compared with control mice

homeostasis/metabolism
• in mice infected with K. pneumonia or following cecal ligation and puncture
• however, response to S. aureus is normal
• in mice infected with K. pneumonia or following cecal ligation and puncture
• following cecal ligation and puncture, mice exhibit improved survival, decreased circulating levels of IL6 and TNFalpha, decreased bacterial dissemination and increased neutrophil infiltration compared with control mice




Genotype
MGI:3826860
cn8
Allelic
Composition
Arg1tm1Pmu/Arg1tm1Pmu
Lyz2tm1(cre)Ifo/?
Genetic
Background
B6.Cg-Arg1tm1Pmu Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arg1tm1Pmu mutation (2 available); any Arg1 mutation (6 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice are resistant to the wasting disease caused by systemic infection with T. gondii
• control mice lose 20% of their body weight by 40 days after T. gondii infection while infected mutant mice have no loss of body weight




Genotype
MGI:5318545
cn9
Allelic
Composition
Cd1d1tm1.1Aben/Cd1d1tm1.1Aben
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.Cg-Cd1d1tm1.1Aben Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd1d1tm1.1Aben mutation (1 available); any Cd1d1 mutation (7 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice exhibit normal development and distribution of NK T cells
• decreased in splenic and liver NK cells after injection of alphaGC
• decreased in splenic NK T cells after injection of alphaGC
• decreased in splenic and liver NK T cells after injection of alphaGC




Genotype
MGI:6192679
cn10
Allelic
Composition
Cybbtm1.1Abk/Cybbtm1.1Abk
Lyz2tm1(cre)Ifo/?
Genetic
Background
B6.Cg-Lyz2tm1(cre)Ifo Cybbtm1.1Abk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cybbtm1.1Abk mutation (1 available); any Cybb mutation (6 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• inguinal adipocytes are smaller in size than controls
• however, in mice fed high fat diet (HFD) the size of visceral adipocytes is similar in both mutant and controls
• increased amount of epididymal fat

behavior/neurological
• HFD-fed mice do not exhibit an impaired freeze response in the fear conditioning assay unlike HFD-fed controls

cellular
• decrease in crown-like structures formed by macrophages in visceral adipose tissue of mice fed HFD as compared to HFD-fed controls

growth/size/body
• decrease in body weight in 5-7 month old mice as compared to controls
• decrease in snout-anus length
• delay in fat accumulation on high fat diet (HFD) as compared to controls
• delay in relative loss of lean mass in first 6 weeks of HFD

hematopoietic system
• decrease in crown-like structures formed by macrophages in visceral adipose tissue of mice fed HFD as compared to HFD-fed controls

homeostasis/metabolism
• delay in fat accumulation on high fat diet (HFD) as compared to controls
• delay in relative loss of lean mass in first 6 weeks of HFD
• glucose levels are lower in HFD-fed mice as compared to HFD-fed controls
• insulin levels are lower in HFD-fed mice as compared to HFD-fed controls
• HDL levels are increased in HFD-fed mice as compared to HFD-fed controls
• total cholesterol levels are lower in both HFD-fed mice and CD-fed mice as compared to controls
• LDL cholesterol levels are lower in HFD-fed mice as compared to HFD-fed controls
• triglyceride levels are lower in HFD-fed mice as compared to HFD-fed controls

immune system
• decrease in crown-like structures formed by macrophages in visceral adipose tissue of mice fed HFD as compared to HFD-fed controls

nervous system




Genotype
MGI:5896660
cn11
Allelic
Composition
Naipctm1Kmma/Naipctm1Kmma
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.Cg-Lyz2tm1(cre)Ifo Naipctm1Kmma
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Naipctm1Kmma mutation (0 available); any Naipc mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice treated with DSS exhibit a slight reduction of colitis in the early phase compared with control mice
• however, there is no protection after 9 days

neoplasm
N
• mice treated with azoxymethane and dextran sulfate sodium exhibit normal tumorigenesis

immune system
• mice treated with DSS exhibit a slight reduction of colitis in the early phase compared with control mice
• however, there is no protection after 9 days




Genotype
MGI:6360685
cn12
Allelic
Composition
Plekhf1tm1.1Caox/Plekhf1tm1.1Caox
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6.Cg-Plekhf1tm1.1Caox Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Plekhf1tm1.1Caox mutation (0 available); any Plekhf1 mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after stimulation with heat-killed and PI (propidium iodide)-labeled E. coli for 1 h, peritoneal macrophages endocytose significantly less E. coli than controls macrophages; endocytosed E. coli do not colocalize with Cav1, unlike in control macrophages
• 1 h after infection macrophages show significantly less endocytosis of viable E. coli or S. aureus than control macrophages, as measured by CFUs
• after incubation with Zymosan or latex beads, mean fluorescence intensity of bone marrow-derived macrophages (BMDMs) is significantly lower than that of control macrophages
• upon LPS stimulation, % of surface TLR4 on BMDMs is significantly higher than that on control macrophages, indicating impaired LPS-activated endocytosis of TLR4

immune system
• after exposure to E. coli, the % of live E. coli counts to initially internalized counts is significantly higher than that in control macrophages, suggesting that bactericidal capacity of macrophages is impaired
• serum IFN-beta levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
• serum IL-6 levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
• serum TNFalpha levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
• upon E. coli or LPS challenge, mice show significantly reduced production of the inflammatory cytokines TNFalpha, IFN-beta, and IL-6 in serum relative to control mice
• upon E. coli or LPS stimulation, macrophages show deceased production of TNFalpha, IFN-beta, and IL-6 relative to control macrophages
• mice are more susceptible to i.p. E. coli infection with significantly higher bacterial loads in spleen and liver, reduced production of TNFalpha, IFN-beta, and IL-6 in serum, and decreased infiltration of inflammatory cells in lung relative to similarly infected control mice
• after i.p. injection with E. coli, all mice die by 3 days after challenge whereas most control mice survive to 5 days post infection

homeostasis/metabolism
• serum IFN-beta levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
• serum IL-6 levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli
• serum TNFalpha levels are significantly reduced at 4 and 8 h after i.p. injection with E. coli

hematopoietic system
• after exposure to E. coli, the % of live E. coli counts to initially internalized counts is significantly higher than that in control macrophages, suggesting that bactericidal capacity of macrophages is impaired

mortality/aging
• after i.p. injection with E. coli, all mice die by 3 days after challenge whereas most control mice survive to 5 days post infection




Genotype
MGI:5882343
cn13
Allelic
Composition
Mapk8tm1Rjd/Mapk8tm1Rjd
Mapk9tm2.1Rjd/Mapk9tm2.1Rjd
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
B6J.Cg-Lyz2tm1(cre)Ifo Mapk9tm2.1Rjd Mapk8tm1Rjd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Mapk8tm1Rjd mutation (0 available); any Mapk8 mutation (40 available)
Mapk9tm2.1Rjd mutation (0 available); any Mapk9 mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• chow-fed mice exhibit a slight but significant reduction in lean mass relative to controls
• however, mice fed a high fat diet (HFD) for 4 weeks show no differences in lean mass relative to HFD-fed controls

homeostasis/metabolism
N
• chow-fed mice exhibit comparable insulin and glucose tolerance and blood concentrations of glucose and insulin relative to chow-fed controls
• HFD-fed mice show comparable diet-induced obesity with no differences in blood glycerol and free fatty acids (FFA) levels relative to HFD-fed controls
• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated cytokine levels relative to chow-fed control mice
• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated chemokine levels relative to chow-fed control mice
• hyperinsulinemic-euglycemic clamp studies revealed that mice fed either a regular chow or a HFD show a significantly enhanced steady-state glucose infusion rate, clamp hepatic glucose production, and insulin-stimulated whole-body glucose turnover relative to similarly-fed control mice
• HFD-fed mice show a significant increase in glucose-induced insulin secretion both in vitro and in vivo relative to HFD-fed controls
• mice are protected from HFD-induced hyperglycemia, unlike HFD-fed controls
• mice are protected from HFD-induced hyperinsulinemia, unlike HFD-fed controls
• HFD-fed mice show significantly reduced gluconeogenesis relative to HFD-fed controls
• HFD-fed mice show improved glucose tolerance relative to HFD-fed controls
• hyperinsulinemic-euglycemic clamp studies revealed that mice fed either a regular chow or a HFD show a significantly enhanced whole-body glycogen plus lipid synthesis relative to similarly-fed control mice
• HFD-fed mice show improved insulin tolerance relative to HFD-fed controls
• hyperinsulinemic-euglycemic clamp studies revealed that increased whole-body insulin sensitivity is due to significant improvements in glucose infusion rates, hepatic insulin action, clamp hepatic glucose production, insulin-stimulated whole body glucose turnover, and whole-body glycogen plus lipid synthesis relative to control mice
• after overnight fasting, HFD-fed mice fail to suppress insulin-stimulated Akt activation in the liver, white adipose tissue and skeletal muscle, unlike similarly treated HFD-fed control mice
• protection of HFD-fed mice against insulin resistance is associated with reduced tissue infiltration by macrophages
• hyperinsulinemic-euglycemic clamp studies revealed that mice fed either a regular chow or a HFD show a significantly enhanced whole-body glycogen plus lipid synthesis relative to similarly-fed control mice
• HFD-fed mice show significantly reduced chemokine expression relative to HFD-fed controls
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of chemokine (Ccl2 and Ccl5) genes relative to control BMDMs

endocrine/exocrine glands
• HFD-fed mice show a significant reduction in pancreatic beta cell proliferation relative to HFD-fed controls
• HFD-fed mice show a significant reduction in pancreatic islet area relative to HFD-fed controls
• however, chow-fed mice show no differences in islet area relative to chow-fed controls
• HFD-fed mice show a significant increase in glucose-induced insulin secretion both in vitro and in vivo relative to HFD-fed controls

immune system
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show reduced M1 differentiation and expression of the cell surface marker CD11c relative to control BMDMs
• however, M2 differentiation appears unaffected
• HFD-fed mice show a significant decrease in the total number of F4/80+ adipose tissue macrophages (ATMs) and reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice also show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• chow-fed mice show no differences in total, M1- or M2-polarized ATM number relative to chow-fed controls
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of M1 marker genes (Ccr7 and Cd11c), chemokines (Ccl2 and Ccl5), and cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
• similar defects are detected in LPS-stimulated macrophages
• HFD-fed mice show significantly reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• however, HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• upon IFN-gamma stimulation, isolated BMDMs show decreased expression of cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated cytokine levels relative to chow-fed control mice
• upon LPS stimulation, chow-fed mice show significantly reduced blood M1-associated chemokine levels relative to chow-fed control mice
• HFD-fed mice show significantly reduced chemokine expression relative to HFD-fed controls
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of chemokine (Ccl2 and Ccl5) genes relative to control BMDMs
• HFD-fed mice show significantly reduced hepatic inflammation relative to HFD-fed controls

hematopoietic system
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show reduced M1 differentiation and expression of the cell surface marker CD11c relative to control BMDMs
• however, M2 differentiation appears unaffected
• HFD-fed mice show a significant decrease in the total number of F4/80+ adipose tissue macrophages (ATMs) and reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice also show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• chow-fed mice show no differences in total, M1- or M2-polarized ATM number relative to chow-fed controls
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show decreased expression of M1 marker genes (Ccr7 and Cd11c), chemokines (Ccl2 and Ccl5), and cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs
• similar defects are detected in LPS-stimulated macrophages
• HFD-fed mice show significantly reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• however, HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• upon IFN-gamma stimulation, isolated BMDMs show decreased expression of cytokine genes (Il1beta, Il6, and Tnf) relative to control BMDMs

cellular
• upon IFN-gamma stimulation, isolated bone marrow-derived macrophages (BMDMs) show reduced M1 differentiation and expression of the cell surface marker CD11c relative to control BMDMs
• however, M2 differentiation appears unaffected
• HFD-fed mice show significantly reduced accumulation of M1-polarized (F4/80+CD11c+CD206-) ATMs in adipose tissue relative to HFD-fed controls
• HFD-fed mice show decreased accumulation of M1 tissue macrophages in the liver relative to HFD-fed controls
• however, HFD-fed mice show no significant difference in the accumulation of M2-polarized ATMs (F4/80+CD11c-CD206+) relative to HFD-fed controls
• HFD-fed mice show a significant reduction in pancreatic beta cell proliferation relative to HFD-fed controls




Genotype
MGI:4455049
cn14
Allelic
Composition
Nr3c1tm2Gsc/Nr3c1tm2Gsc
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
C.129P2-Lyz2tm1(cre)Ifo Nr3c1tm2Gsc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Nr3c1tm2Gsc mutation (1 available); any Nr3c1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
N
• bone formation rate with prednisolone treatment for 2 weeks is reduced in mutants and controls




Genotype
MGI:4819947
cn15
Allelic
Composition
Il1rntm1.1Cga/Il1rntm1.1Cga
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
D1.Cg-Il1rntm1.1Cga Lyz2tm1(cre)Ifo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Il1rntm1.1Cga mutation (0 available); any Il1rn mutation (9 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in draining lymph node cells from collagen-treated wild-type mice

immune system
• in draining lymph node cells from collagen-treated wild-type mice
• myeloid cells from collage-treated mice exhibit increased CXCL1 and CXCL2 production compared with wild-type mice
• in draining lymph node cells from collagen-treated wild-type mice
• in myeloid cells from the ankles of collagen-treated mice
• in myeloid cells from the ankles of collagen-treated mice
• in draining lymph node cells from collagen-treated wild-type mice
• in myeloid cells from the ankles of collagen-treated mice
• in myeloid cells from the ankles of collage-treated mice
• collagen treated mice exhibit earlier and more severe arthritis with increased number of paws affected, inflammation, cartilage erosion, and neutrophil infiltration compared with similarly treated wild-type mice
• draining lymph node cells from collagen-stimulated mice exhibit increased T cell proliferation, and IFN-gamma and IL17 production compared with similarly treated wild-type cells
• myeloid cells from the ankles of collagen-treated mice exhibit increased IL1b, IL6, IFNgamma, IL17, CXCL1, and CXCL2 production compared with wild-type mice

skeleton
• collagen treated mice exhibit earlier and more severe arthritis with increased number of paws affected, inflammation, cartilage erosion, and neutrophil infiltration compared with similarly treated wild-type mice
• draining lymph node cells from collagen-stimulated mice exhibit increased T cell proliferation, and IFN-gamma and IL17 production compared with similarly treated wild-type cells
• myeloid cells from the ankles of collagen-treated mice exhibit increased IL1b, IL6, IFNgamma, IL17, CXCL1, and CXCL2 production compared with wild-type mice

hematopoietic system
• in draining lymph node cells from collagen-treated wild-type mice




Genotype
MGI:3846105
cn16
Allelic
Composition
Hmox1tm1.1Gkl/Hmox1tm1.1Gkl
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * 129P2/OlaHsd * BALB/cJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmox1tm1.1Gkl mutation (1 available); any Hmox1 mutation (10 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Hmox1tm1.1Gkl/Hmox1tm1.1Gkl Lyz2tm1(cre)Ifo/Lyz2+ mice show decreased susceptibility to L. monocytogenes infection

mortality/aging
• mice infected with L. monocytogenes and treated with polyI:C exhibit decreased IFN-beta production and mortality compared to similarly treated wild-type mice

immune system
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
• in MOG-treated mice
• in MOG-treated mice
• MOG-treated mice exhibit an increase in CD4+ T cells compared to in similarly treated wild-type mice
• MOG-treated mice exhibit a 5-fold increase in the number of IL17-producing CD4+ T cells and a 2-fold increase in IFN-gamma-producing CD4+ T cells compared to similarly treated wild-type mice
• in MOG-treated mice
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
• polyI:C- or LPS-stimulated macrophages or mice stimulated with LPS and infected with L. monocytogenes produce less IFN-beta than similarly treated wild-type cells or mice
• macrophages infected with the Sendai virus produce less IFN-beta than similarly treated wild-type cells
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
• mice exhibit exacerbated experimental autoimmune encephalomyelitis (EAE) and do not exhibit suppression of EAE symptoms and IFN-beta production by polyI:C treatment unlike similarly treated wild-type mice
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice
• MOG-treated mice exhibit more cellular infiltration with increased CD4+ and CD8+ T cells, macrophages, B cells, and granulocytes and increased demyelination throughout the spinal cord compared to similarly treated wild-type mice
• MOG-treated mice exhibit a 5-fold increase in the number of IL17-producing CD4+ T cells and a 2-fold increase in IFN-gamma-producing CD4+ T cells compared to similarly treated wild-type mice
• mice infected with L. monocytogenes and treated with polyI:C exhibit decreased IFN-beta production and mortality compared to similarly treated wild-type mice
• macrophages infected with the Sendai virus produce less IFN-beta than similarly treated wild-type cells

homeostasis/metabolism
• MOG-treated mice exhibit increased IFN-gamma and TNF serum levels compared to similarly treated wild-type mice

hematopoietic system
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice
• in MOG-treated mice
• in MOG-treated mice
• MOG-treated mice exhibit an increase in CD4+ T cells compared to in similarly treated wild-type mice
• MOG-treated mice exhibit a 5-fold increase in the number of IL17-producing CD4+ T cells and a 2-fold increase in IFN-gamma-producing CD4+ T cells compared to similarly treated wild-type mice
• in MOG-treated mice

cellular
• MOG-treated mice exhibit a 4-fold increase in splenocyte proliferation compared to similarly treated wild-type mice




Genotype
MGI:3527247
cn17
Allelic
Composition
Tnftm1.1Sned/Tnftm1.1Sned
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Tnftm1.1Sned mutation (0 available); any Tnf mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• mutants infected with Listeria monocytogenes developed large, confluent inflammatory necrotic areas with many Mac-1 and Gr1-positive cells
• no liver necrosis, only infiltrating cells, were detected in mutants with ConA induced autoimmune hepatitis

mortality/aging
• died within 4 days after Listeria monocytogenes infection whereas controls survived

immune system
• serum TNF levels were dramatically reduced in mutants injected with LPS, with TNF production decreased by 100-fold in macrophages
• induction of MCP-1 was reduced in spleens of mutants infected with Listeria monocytogenes
• increased resistance to liver injury after ConA-induced autoimmune hepatitis
• fully resistant to lipopolysaccharide (LPS)/D-Gal induced septic shock
• protected from toxic shock induced by enterotoxin B, a superantigen from S. aureus
• loss of resistance against Listeria monocytogenes, developing uncontrolled infection, leading to death within 4 days and a 3-4 log increase in bacterial load in the liver and spleen

liver/biliary system
• mutants infected with Listeria monocytogenes developed large, confluent inflammatory necrotic areas with many Mac-1 and Gr1-positive cells
• no liver necrosis, only infiltrating cells, were detected in mutants with ConA induced autoimmune hepatitis

homeostasis/metabolism
• serum TNF levels were dramatically reduced in mutants injected with LPS, with TNF production decreased by 100-fold in macrophages




Genotype
MGI:6158666
cn18
Allelic
Composition
Lyz2tm1(cre)Ifo/Lyz2+
Pdcd10tm1Wami/Pdcd10tm1Wami
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Pdcd10tm1Wami mutation (0 available); any Pdcd10 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• after renal ischemia-reperfusion experiments

hematopoietic system
• increased degranulation
• increased degranulation

homeostasis/metabolism
• in serum after renal ischemia-reperfusion experiments

immune system
• increased degranulation
• increased degranulation

renal/urinary system
• after renal ischemia-reperfusion experiments




Genotype
MGI:4838306
cn19
Allelic
Composition
Cfptm2.1Song/Cfptm2.1Song
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cfptm2.1Song mutation (0 available); any Cfp mutation (5 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• LPS-induced alternative pathway (AP) complement activation is impaired unlike in wild-type mice

skeleton




Genotype
MGI:3850053
cn20
Allelic
Composition
Il1r1tm1Roml/Il1r1tm1Roml
Nlrp3tm1Hhf/Nlrp3+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Il1r1tm1Roml mutation (2 available); any Il1r1 mutation (25 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Nlrp3tm1Hhf mutation (1 available); any Nlrp3 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• postnatal lethality does not occur to mice on a IL-1 receptor null background

immune system
• variable skin inflammation is observed

integument
• variable skin inflammation is observed




Genotype
MGI:3850059
cn21
Allelic
Composition
Nlrp3tm1Flv/Nlrp3tm1Hhf
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Nlrp3tm1Flv mutation (0 available); any Nlrp3 mutation (40 available)
Nlrp3tm1Hhf mutation (1 available); any Nlrp3 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die between 2 and 14 days after birth probably due to multisystem organ failure secondary to inflammation and necrosis
• genotype demonstrates inflammatory disease of the conditional allele does not require presence of wild-type allele

immune system
• mice have pronounced leukocytic infiltrates in skin, liver, spleen, joint, sinus, conjunctiva, bone marrow, and tongue that are mainly neutrophilic




Genotype
MGI:5570434
cn22
Allelic
Composition
Ptgestm1.1Gaf/Ptgestm1.1Gaf
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Ptgestm1.1Gaf mutation (0 available); any Ptges mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• following wire injury, mice exhibit decreased intima to media ratio and stenosis percent with increased leukocyte recruitment compared with control mice
• decreased LPS-stimulated prostaglandin E2
• however, LPS-stimulated prostaglandin D2 levels are normal
• increased LPS-stimulated prostaglandin I2 levels

immune system
• increased leukocyte recruitment following wire injury
• increased leukocyte recruitment following wire injury

cardiovascular system
• following wire injury, mice exhibit decreased intima to media ratio and stenosis percent with increased leukocyte recruitment compared with control mice

hematopoietic system
• increased leukocyte recruitment following wire injury
• increased leukocyte recruitment following wire injury




Genotype
MGI:3850058
cn23
Allelic
Composition
Nlrp3tm1Hhf/Nlrp3+
Pycardtm1Flv/Pycardtm1Flv
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Nlrp3tm1Hhf mutation (1 available); any Nlrp3 mutation (40 available)
Pycardtm1Flv mutation (0 available); any Pycard mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice appear phenotypically normal and do not develop the inflammatory disease that conditional heterozygotes develop on an intact Pycard background




Genotype
MGI:6093456
cn24
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-CAMK2G*T287D,-EGFP)Whua/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-CAMK2G*T287D,-EGFP)Whua mutation (0 available); any Gt(ROSA)26Sor mutation (512 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• mice treated with dextran sodium sulfate (DSS) to induce colitis show similar colitis-induced injury as controls, with slightly greater weight loss but similar colon shortening and splenic enlargement




Genotype
MGI:3811199
cn25
Allelic
Composition
Mef2ctm1Jjs/Mef2ctm1Jjs
Mir223tm1Fcam/Mir223tm1Fcam
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Mef2ctm1Jjs mutation (1 available); any Mef2c mutation (4 available)
Mir223tm1Fcam mutation (1 available); any Mir223 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• neutrophils exhibit an unusual hypermature morphology characterized by nuclear hypersegmentation and blebbing
• neutrophil numbers are normal in these mice unlike the increased numbers observed in Mirn223tm1Fcam homozygotes
• neutorphils are hypersensitive to activating stimuli
• neutrophils have higher oxidative burst than controls upon low-dose PMA stimulation
• neutrophils display higher killing when co-cultured with Candida albicans

hematopoietic system
• neutrophils exhibit an unusual hypermature morphology characterized by nuclear hypersegmentation and blebbing
• neutrophil numbers are normal in these mice unlike the increased numbers observed in Mirn223tm1Fcam homozygotes
• neutorphils are hypersensitive to activating stimuli
• neutrophils have higher oxidative burst than controls upon low-dose PMA stimulation
• neutrophils display higher killing when co-cultured with Candida albicans

cellular
• neutrophils exhibit an unusual hypermature morphology characterized by nuclear hypersegmentation and blebbing




Genotype
MGI:3051636
cn26
Allelic
Composition
Socs3tm1Ayos/Socs3tm1Ayos
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Socs3tm1Ayos mutation (2 available); any Socs3 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mutants are more resistant to LPS induced endotoxin shock




Genotype
MGI:3844880
cn27
Allelic
Composition
Rfx5tm1Ifo/Rfx5tm1.1Ifo
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6 * C.B-20
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Rfx5tm1.1Ifo mutation (0 available); any Rfx5 mutation (22 available)
Rfx5tm1Ifo mutation (1 available); any Rfx5 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• only 6.2% of bone marrow derived macrophages express MHC-II on the surface compared to 30% of controls
• incubation with IFN-gamma increases percentage to 19% which is much less than 72% of wild-type macrophages

hematopoietic system
• only 6.2% of bone marrow derived macrophages express MHC-II on the surface compared to 30% of controls
• incubation with IFN-gamma increases percentage to 19% which is much less than 72% of wild-type macrophages




Genotype
MGI:5444295
cn28
Allelic
Composition
Vegfatm2Gne/Vegfatm2Gne
Lyz2tm1(cre)Ifo/Lyz2+
Tg(KRT14-cre)1Cgn/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Tg(KRT14-cre)1Cgn mutation (2 available)
Vegfatm2Gne mutation (0 available); any Vegfa mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• during the early and middle phases of wound healing, mice exhibit reduced formation and vascularization of granulation tissue compared with control mice




Genotype
MGI:3027959
cn29
Allelic
Composition
Pcyt1atm1Irt/Pcyt1atm1Irt
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Pcyt1atm1Irt mutation (1 available); any Pcyt1a mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• normal numbers of peritoneal macrophage
• no CTP:phosphocholine cytidylyltransferase alpha produced
• CTP:phosphocholine cytidylyltransferase, beta isoform upregulated
• severely reduced conversion of free cholesterol to phosphatidylcholine
• increased free cholesterol load leads to macrophage cell death

hematopoietic system
• normal numbers of peritoneal macrophage
• no CTP:phosphocholine cytidylyltransferase alpha produced
• CTP:phosphocholine cytidylyltransferase, beta isoform upregulated
• severely reduced conversion of free cholesterol to phosphatidylcholine
• increased free cholesterol load leads to macrophage cell death




Genotype
MGI:3810470
cn30
Allelic
Composition
Adam17tm1Bbl/Adam17tm1Bbl
Lyz2tm1(cre)Ifo/0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adam17tm1Bbl mutation (0 available); any Adam17 mutation (40 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• TNF levels in the serum of mice expressing Cre are lower by more than two thirds compared to controls 3 hours after LPS injection

immune system
• LPS stimulated release of TNF from macrophages is strongly reduced in these mice
• TNF levels in the serum of mice expressing Cre are lower by more than two thirds compared to controls 3 hours after LPS injection
• two weeks after induction of Cre recombinase, mice are more resistant to endotoxin shock than in controls
• 10 of 13 mice survive endotoxin induction with LPS and D-galactosamine while 11 of 13 controls die within 8 hours of injection

hematopoietic system
• LPS stimulated release of TNF from macrophages is strongly reduced in these mice




Genotype
MGI:4868712
cn31
Allelic
Composition
Cflartm1.1Pope/Cflartm1.2Pope
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cflartm1.1Pope mutation (0 available); any Cflar mutation (4 available)
Cflartm1.2Pope mutation (0 available); any Cflar mutation (4 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% mortality before 32 weeks of age
• mortality increases to 80% by 3-5 weeks if Lyz2tm1(cre)Ifo is homozygous

growth/size/body
• 50% reduction in body size

hematopoietic system
• increased number of neutrophiles
• decrease in thymocytes
• loss of a distinct medulla and cortex
• reduced bone marrow erythropoiesis
• splenic extramedullary myelopoiesis
• expanded number of neutrophiles
• reduced erythropoiesis
• thrombocytosis
• decreased percentage but not in absolute numbers in peripheral blood
• absolute number of B cells reduced in the spleen
• decreased percentage but not in absolute numbers in peripheral blood
• decreased percentage in peripheral blood
• slightly increased in absolute numbers in peripheral blood
• reduced numbers in the peritoneal cavity
• 5 fold increase in leukocytes in peripheral blood
• increased more than 10 fold
• accumulate in the lung alveolar spaces and around the large blood vessels
• accumulate in the small intestine, particularly the jejunum
• increased numbers in the peritoneal cavity
• increased more than 10 fold
• increase of the inflammatory subclass
• disrupted architecture
• granulocyte infiltration
• infiltration of neutrophiles
• reduction in macrophage number
• splenomegaly with loss of lymphoid follicles
• normal cell number but composition includes more large immature and myeloid cells and fewer lymphocytes
• loss of lymphoid follicles
• reduction in macrophage number

immune system
• increased number of neutrophiles
• decrease in thymocytes
• loss of a distinct medulla and cortex
• splenic extramedullary myelopoiesis
• decreased percentage but not in absolute numbers in peripheral blood
• absolute number of B cells reduced in the spleen
• decreased percentage but not in absolute numbers in peripheral blood
• decreased percentage in peripheral blood
• slightly increased in absolute numbers in peripheral blood
• reduced numbers in the peritoneal cavity
• 5 fold increase in leukocytes in peripheral blood
• increased more than 10 fold
• accumulate in the lung alveolar spaces and around the large blood vessels
• accumulate in the small intestine, particularly the jejunum
• increased numbers in the peritoneal cavity
• increased more than 10 fold
• increase of the inflammatory subclass
• disrupted architecture
• granulocyte infiltration
• infiltration of neutrophiles
• reduction in macrophage number
• splenomegaly with loss of lymphoid follicles
• normal cell number but composition includes more large immature and myeloid cells and fewer lymphocytes
• loss of lymphoid follicles
• reduction in macrophage number
• loss of lymphoid follicles
• infiltration of neutrophiles
• 4fewer macrophage

endocrine/exocrine glands
• increased number of neutrophiles
• decrease in thymocytes
• loss of a distinct medulla and cortex




Genotype
MGI:6287982
cn32
Allelic
Composition
Rb1cc1tm1.1Guan/Rb1cc1tm1.1Guan
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Rb1cc1tm1.1Guan mutation (0 available); any Rb1cc1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice do not develop lupus-like disease and do not exhibit an increase in anti-double stranded DNA antibodies or in anti-nuclear antibodies, do not show glomerular immune complex deposition, show normal serum creatinine levels and cytokine levels, and normal clearance of engulfed, dying cells




Genotype
MGI:5504638
cn33
Allelic
Composition
P4hbtm1.1Geno/P4hbtm1.2Geno
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
P4hbtm1.1Geno mutation (0 available); any P4hb mutation (24 available)
P4hbtm1.2Geno mutation (0 available); any P4hb mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• to the inflamed endothelium
• during TNF-alpha-induced inflammation, mice exhibit increased rolling influx, reduced percentage of crawling cells among adherent neutrophils and reduced number of adherent neutrophils to the inflamed endothelium
• neutrophils exhibit reduced neutrophil adhesion to ICAM-1-coated surface compared with wild-type cells

hematopoietic system
• to the inflamed endothelium
• during TNF-alpha-induced inflammation, mice exhibit increased rolling influx, reduced percentage of crawling cells among adherent neutrophils and reduced number of adherent neutrophils to the inflamed endothelium
• neutrophils exhibit reduced neutrophil adhesion to ICAM-1-coated surface compared with wild-type cells




Genotype
MGI:4453320
cn34
Allelic
Composition
Ltbrtm1Avt/Ltbrtm1Avt
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ltbrtm1Avt mutation (0 available); any Ltbr mutation (4 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• display increased bacterial titers in the blood and feces
• despite this mice survive the infection




Genotype
MGI:5487464
cn35
Allelic
Composition
Sqstm1tm2.1Jmos/Sqstm1tm2.1Jmos
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Sqstm1tm2.1Jmos mutation (0 available); any Sqstm1 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
N
• mice fed standard chow or a high fat diet exhibit normal body weight and composition

homeostasis/metabolism
N
• mice fed standard chow or a high fat diet exhibit normal glucose tolerance

cellular
N
• brown adipose tissue exhibits normal mitochondrial function (measured by cox activity)




Genotype
MGI:6144087
cn36
Allelic
Composition
Lyz2tm1(cre)Ifo/Lyz2tm1(cre)Ifo
Nrrostm1Wouy/Nrrostm1Wouy
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Nrrostm1Wouy mutation (0 available); any Nrros mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increased migration into CNS in myelin oligodendrocyte glycoprotein MOG-CFA-induced EAE experiments
• significantly increased ROS production from CNS-infiltrating leukocytes in MOG-CFA-induced EAE experiments
• significantly increased malondialdehyde levels in CNS tissue in MOG-CFA-induced EAE experiments

hematopoietic system
• increased migration into CNS in myelin oligodendrocyte glycoprotein MOG-CFA-induced EAE experiments

immune system
• increased migration into CNS in myelin oligodendrocyte glycoprotein MOG-CFA-induced EAE experiments
• increased disease severity (lesions in central nervous system (CNS)) and high mortality in myelin oligodendrocyte glycoprotein (MOG)35-55-complete Freunds adjuvant (CFA)-induced EAE experiments
• when treated with reactive oxygen species (ROS) scavengers after EAE induction with MOG-CFA




Genotype
MGI:5563539
cn37
Allelic
Composition
Hmgb1tm1.1Ttg/Hmgb1tm1.1Ttg
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmgb1tm1.1Ttg mutation (0 available); any Hmgb1 mutation (8 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• normal myeloid lineage and in vitro M1 and M2 macrophage differentiation
• decrease in autophagosome formation in response to lipopolysaccharide injection or bacterial infection
• with TLR stimulation and pan-caspase inhibition treatments
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy

immune system
• decrease in autophagosome formation in response to lipopolysaccharide injection or bacterial infection
• with TLR stimulation and pan-caspase inhibition treatments
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
• in cultured macrophages stimulated with LPS and ATP
• in cultured macrophages stimulated with LPS and ATP
• along with massive lung tissue destruction upon lipopoysaccharide injection

homeostasis/metabolism
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway

cellular
• with TLR stimulation and pan-caspase inhibition treatments
• higher in vitro macrophage cell death after lipopolysaccharide injection
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy




Genotype
MGI:5470074
cn38
Allelic
Composition
Stk11tm1Keis/Stk11tm1Keis
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Stk11tm1Keis mutation (0 available); any Stk11 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• bone marrow derived macrophage show increased levels of LPS induced IL-10 mRNA and no further effect from addition PGE2 stimulation

homeostasis/metabolism
• bone marrow derived macrophage show increased levels of LPS induced IL-10 mRNA and no further effect from addition PGE2 stimulation




Genotype
MGI:5314236
cn39
Allelic
Composition
Syktm1.1Nns/Syktm1.1Nns
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Syktm1.1Nns mutation (0 available); any Syk mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice exhibit normal perinatal survival

immune system
N
• mice exhibit normal lymphatic vessels with normal integrity

homeostasis/metabolism
N
• mice do not exhibit edema




Genotype
MGI:5775293
cn40
Allelic
Composition
Engtm2.1Hma/Engtm2.1Hma
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Engtm2.1Hma mutation (1 available); any Eng mutation (14 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen treated mice do not develop arteriovenous malformations in response to AAV-VEGF injection into the basal ganglia at 8-10 weeks of age or around the ear tag wound




Genotype
MGI:6287976
cn41
Allelic
Composition
Becn1tm1Ebr/Becn1tm1Ebr
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Becn1tm1Ebr mutation (0 available); any Becn1 mutation (27 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice appear normal at weaning but fail to gain weight

hematopoietic system
• increase in levels of circulating neutrophils
• increase in levels of circulating lymphocytes
• increase in levels of circulating monocytes
• spleens show increased expression of interferon signature genes such as Ddx58 and Isg95
• IgG deposition in the glomeruli of kidneys
• macrophages exhibit an acute elevation of proinflammatory cytokines IL-1beta, IL-6, and IP-10, but not IL-10, in response to ingesting dying cells that is not seen in control macrophages
• however, neither bone marrow-derived macrophages nor peritoneal exudate macrophages from 52 week old mice show any defects in the engulfment of dying cells in vitro indicating normal phagocytic capacity

homeostasis/metabolism
• levels of CXCL1, CCL4 and CCL2 are increased in 52-week old mice

immune system
• increase in levels of circulating neutrophils
• increase in levels of circulating lymphocytes
• increase in levels of circulating monocytes
• spleens show increased expression of interferon signature genes such as Ddx58 and Isg95
• IgG deposition in the glomeruli of kidneys
• macrophages exhibit an acute elevation of proinflammatory cytokines IL-1beta, IL-6, and IP-10, but not IL-10, in response to ingesting dying cells that is not seen in control macrophages
• however, neither bone marrow-derived macrophages nor peritoneal exudate macrophages from 52 week old mice show any defects in the engulfment of dying cells in vitro indicating normal phagocytic capacity
• levels of CXCL1, CCL4 and CCL2 are increased in 52-week old mice
• mice develop a systemic lupus erythematosus-like disease (SLE)
• increase in serum levels of a broad array of antibodies against autoantigens commonly associated with SLE
• kidneys from aged mice show endocapillary proliferative glomerulonephritis

renal/urinary system
• mice show indications of kidney damage and show increased functional markers of kidney injury
• IgG and complement C1q deposition in the glomeruli of kidneys
• kidneys from aged mice show endocapillary proliferative glomerulonephritis




Genotype
MGI:5581947
cn42
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (22 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:4418465
cn43
Allelic
Composition
Hif1atm3Rsjo/Hif1atm3Rsjo
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm3Rsjo mutation (3 available); any Hif1a mutation (11 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells
• macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells
• bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice
• macrophages lack homotypic adhesion unlike wild-type cells
• macrophage capacity to invade matrigel is severely defective compared with wild-type mice
• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells
• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells
• in LPS-treated macrophages
• TPA-treated ears exhibit reduced inflammatory infiltration and edema compared with similarly treated wild-type cells
• following disruption of barrier function with 5% SDS (chronic cutaneous inflammation), mice fail to exhibit an inflammatory response as in similarly treated wild-type mice

homeostasis/metabolism
• following oxygen-induced retinopathy, mice exhibit decreased repair of retinal damage compared with similarly treated wild-type mice
• CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells

skeleton

cellular
• macrophage capacity to invade matrigel is severely defective compared with wild-type mice
• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells
• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells

hematopoietic system
• CD44hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells
• macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells
• bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice
• macrophages lack homotypic adhesion unlike wild-type cells
• macrophage capacity to invade matrigel is severely defective compared with wild-type mice
• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells
• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells




Genotype
MGI:5581946
cn44
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (22 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:4418500
cn45
Allelic
Composition
Hif1atm3Rsjo/Hif1atm3Rsjo
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm3Rsjo mutation (3 available); any Hif1a mutation (11 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in LPS-treated mice compared with similarly treated wild-type mice

immune system
• 4 hours after LPS treatment
• 4 hours after LPS treatment
• 4 hours after LPS treatment
• 1.5 hrs after LPS treatment
• 1.5 and 4 hrs after LPS treatment
• LPS-treated mice exhibit less hypothermia, hypotension, and mortality; improved hemodynamic parameter, shock index, and heart rate to systolic blood pressure; and decreased macrophage cytokine production (TNF-alpha, IL6, IL12, IL1a, and IL1b) compared with similarly treated wild-type mice

homeostasis/metabolism
• LPS-treated mice develop less hypothermia compared with similarly treated wild-type mice
• in LPS-treated mice compared with similarly treated wild-type mice

cardiovascular system
• LPS-treated mice develop less hypotension compared with similarly treated wild-type mice




Genotype
MGI:3699187
cn46
Allelic
Composition
Gbatm1Clk/Gbatm1.1Clk
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gbatm1.1Clk mutation (2 available); any Gba mutation (27 available)
Gbatm1Clk mutation (1 available); any Gba mutation (27 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• tissue glucocerebrosidase activity is reduced to ~30-50% of control levels in all tissues




Genotype
MGI:6196858
cn47
Allelic
Composition
Gt(ROSA)26Sortm1(OVAL/fla,GFP)Vnce/Gt(ROSA)26Sor+
Lyz2tm1(cre)Ifo/Lyz2+
Pycardtm1Vmd/Pycardtm1Vmd
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(OVAL/fla,GFP)Vnce mutation (0 available); any Gt(ROSA)26Sor mutation (512 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Pycardtm1Vmd mutation (1 available); any Pycard mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
N
• mice show normal weight gain at 10 weeks of age

homeostasis/metabolism
• slight increase in IFN-gamma levels
• slight increase in IL-6 levels
• slight increase in TNF levels

immune system
N
• mice show no joint inflammation at 10 weeks of age, cytokine levels (such as IL-1 alpha, IL-1 beta, and MCP-1) are severely reduced, and the autoinflammatory disease seen in Gt(ROSA)26Sortm1(OVAL/fla-GFP)Vnce and Lyz2tm1(cre)Ifo expressing mice is almost entirely ameliorated
• slight increase in IFN-gamma levels
• slight increase in IL-6 levels
• slight increase in TNF levels




Genotype
MGI:4829853
cn48
Allelic
Composition
Cdkn2btm1Wff/Cdkn2btm1Wff
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2btm1Wff mutation (0 available); any Cdkn2b mutation (3 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• an increased frequency of granulocyte-monocyte progenitors in the bone marrow
• bone marrow cells demonstrate a significant increase in both mature myeloid, immature myeloid and monocytic cells
• a decreased frequency of megakaryocyte-erythroid progenitors
• a decreased frequency of megakaryocyte-erythroid progenitors
• show a 2-fold increase in the numbers of circulating monocytes at 5 to 7 months of age

immune system
• bone marrow cells demonstrate a significant increase in both mature myeloid, immature myeloid and monocytic cells
• show a 2-fold increase in the numbers of circulating monocytes at 5 to 7 months of age




Genotype
MGI:3771395
cn49
Allelic
Composition
Il12btm1Jm/Il12btm1Jm
Stat3tm2Aki/Stat3tm2Aki
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Il12btm1Jm mutation (4 available); any Il12b mutation (21 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Stat3tm2Aki mutation (1 available); any Stat3 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• mice exhibit normal Th1 responses and do not develop colitis, unlike Stat3 null mice




Genotype
MGI:5298874
cn50
Allelic
Composition
Esr2tm1.1Pcn/Esr2tm1.1Pcn
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr2tm1.1Pcn mutation (0 available); any Esr2 mutation (25 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in ovariectomized mice treated with 17beta-estradiol due to reduced re-epithelialization of the wound




Genotype
MGI:4415250
cn51
Allelic
Composition
Itgamtm1Myd/Itgamtm1Myd
Syktm1Tyb/Syktm1.2Tara
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgamtm1Myd mutation (1 available); any Itgam mutation (2 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Syktm1.2Tara mutation (1 available); any Syk mutation (28 available)
Syktm1Tyb mutation (0 available); any Syk mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• S. aureus-infected mice exhibit an increased in viable S. aureus compared to in similarly treated wild-type mice

hematopoietic system
• S. aureus-infected mice exhibit an increased in viable S. aureus compared to in similarly treated wild-type mice




Genotype
MGI:5688877
cn52
Allelic
Composition
Itgb3tm1Hyn/Itgb3tm1.1Wlbcr
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgb3tm1.1Wlbcr mutation (1 available); any Itgb3 mutation (30 available)
Itgb3tm1Hyn mutation (6 available); any Itgb3 mutation (30 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• osteoclasts exhibit decreased fusion during differentiation

hematopoietic system
• decreased size of multinucleate osteoclasts as compared to controls
• osteoclasts exhibit decreased fusion during differentiation
• osteoclasts exhibit decreased fusion during differentiation
• numbers of osteoclasts are decreased during differentiation

homeostasis/metabolism
• decreased levels of serum type I collagen as compared to wild type

immune system
• decreased size of multinucleate osteoclasts as compared to controls
• osteoclasts exhibit decreased fusion during differentiation
• osteoclasts exhibit decreased fusion during differentiation
• numbers of osteoclasts are decreased during differentiation

skeleton
• decreased size of multinucleate osteoclasts as compared to controls
• osteoclasts exhibit decreased fusion during differentiation
• osteoclasts exhibit decreased fusion during differentiation
• numbers of osteoclasts are decreased during differentiation
• increased bone mineral density is found in 2 and 6 month old mice as compared to controls
• increased trabecular bone volume in femoral and tibial bones

neoplasm
• macrophage infiltration is decreased in implanted subcutaneous tumors as compared to tumor implanted controls
• implanted melanoma cells have an increased live cell mass and volume as compared to tumor implanted controls




Genotype
MGI:4415249
cn53
Allelic
Composition
Syktm1Tyb/Syktm1.2Tara
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Syktm1.2Tara mutation (1 available); any Syk mutation (28 available)
Syktm1Tyb mutation (0 available); any Syk mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• migration of neutrophils to the cite of bacterial infection is enhanced compared to in similarly treated wild-type mice
• S. aureus-infected mice exhibit a 3- to 4-fold increased in viable S. aureus compared to in similarly treated wild-type mice

hematopoietic system
• migration of neutrophils to the cite of bacterial infection is enhanced compared to in similarly treated wild-type mice
• S. aureus-infected mice exhibit a 3- to 4-fold increased in viable S. aureus compared to in similarly treated wild-type mice




Genotype
MGI:3759847
cn54
Allelic
Composition
Itgavtm2Hyn/Itgavtm2.1Hyn
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgavtm2.1Hyn mutation (0 available); any Itgav mutation (8 available)
Itgavtm2Hyn mutation (2 available); any Itgav mutation (8 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• macrophages exhibit impaired ability to phagocytose and remove apoptotic cells

immune system
• macrophages exhibit impaired ability to phagocytose and remove apoptotic cells
• mice develop colitis similar to Itgavtm2Hyn/Itgavtm2.1Hyn;Tg(Tek-cre)1Ywa mice with similar histology and proinflammatory cytokine expression but at a lower rate (30% compared to 100% of Itgavtm2Hyn/Itgavtm2.1Hyn;Tg(Tek-cre)1Ywa mice at 40 weeks)
• mice contain higher levels of autoantibodies including ones against tropomyosin, phosphotidylserine, double-stranded DNA and anti-nuclear antibodies compared to in Itgavtm2Hyn heterozygote controls

digestive/alimentary system
• mice develop colitis similar to Itgavtm2Hyn/Itgavtm2.1Hyn;Tg(Tek-cre)1Ywa mice with similar histology and proinflammatory cytokine expression but at a lower rate (30% compared to 100% of Itgavtm2Hyn/Itgavtm2.1Hyn;Tg(Tek-cre)1Ywa mice at 40 weeks)

hematopoietic system
• macrophages exhibit impaired ability to phagocytose and remove apoptotic cells




Genotype
MGI:3839885
cn55
Allelic
Composition
Kmt2atm1.1Erns/Kmt2atm1.1Erns
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt2atm1.1Erns mutation (0 available); any Kmt2a mutation (79 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice exhibit normally differentiating T, B, and myeloid cells




Genotype
MGI:4418464
cn56
Allelic
Composition
Vhltm1Jae/Vhltm1Jae
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Vhltm1Jae mutation (2 available); any Vhl mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• TPA-treated ears exhibit increased edema and inflammatory infiltration compared with similarly treated wild-type ears




Genotype
MGI:4836609
cn57
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Ptentm1Hwu mutation (4 available); any Pten mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• macrophage recruitment to inflamed lungs is increased
• number of resident alveolar macrophages in unchallenged mutants is increased by more than 60% percent compared to wild-type
• neutrophils isolated from bone marrow live longer than wild-type neutrophils (J:114699)
• neutrophils exhibit enhanced ruffling in response to the chemoattractant fMLP or IL-8 (J:145331)
• polarized neutrophils exhibit a considerable increase in multiple pseudopodia compared to wild-type mice (J:145331)
• neutrophils show more diffuse F-actin localization at the leading edge or pseudopodia than wild-type neutrophils (J:145331)
• fMLP-stimulated, but not PMA-stimulated, neutrophils exhibit increased and prolonged superoxide production compared to wild-type neutrophils (J:145331)
• neutrophils exhibit enhanced transwell chemotaxis toward fMLP, IL-8 or C5a (J:145331)
• neutrophils are more active and move faster than wild-type neutrophils but lack some of the directionality of wild-type neutrophils (J:145331)
• in a model of peritonitis, neutrophil recruitment at sites of inflammation is increased in mutants compared to wild-type mice (J:145331)
• in a model of bacterial pneumonia, apoptosis of lung recruited neutrophils is reduced in mutants compared to wild-type mice (J:148947)
• neutrophils exhibit enhanced bacteria-killing capacity in a model of bacterial pneumonia (J:148947)
• neutrophils have an increased phagocytic index compared to wild-type in a model of bacterial pneumonia (J:148947)
• neutrophils exhibit enhanced E.coli and zymosan-induced phagocytosis-associated superoxide production (J:148947)
• in a bacterial pneumonia model in which mutants are intratracheally infected with E.coli to induce lung inflammation, mutants exhibit an increase in bacteria-induced neutrophil recruitment compared to controls
• mutants treated with the chemotherapeutic drug, cyclophosphamide, to induce neutropenia, exhibit fewer neutrophils in the lungs than untreated mutants, but more neutrophils than drug treated wild-type mice
• increase in cytokine/chemokine concentrations in inflamed lungs of E.coli infected mutants due to increased numbers of resident alveolar macrophages and not due to enhanced capability of macrophages to produce cytokines or chemokines
• mutants develop more severe lung inflammation in response to bacterial pneumonia than controls
• induction of neutropenia in mutants with the chemotherapeutic drug, cyclophosphamide, results in enhanced neutrophil accumulation in the lungs leading to better clearance of instilled bacteria and accelerated resolution of bacteria-induced lung inflammation
• mutants made neutropenic with the chemotherapeutic drug, cyclophosphamide, exhibit decreased mortality after E.coli challenge compared to wild-type mice due to enhanced neutrophil accumulation in the lungs (50% survival for mutants compared to 7% survival for wild-type mice)
• mutants intratracheally infected with E.coli exhibit increased neutrophil recruitment to lungs and increased lung inflammation, pulmonary edema, and increased susceptibility to death compared to controls
• mutants exhibit an increase in pneumonia-associated death rate compared to wild-type mice, with only 50% of mutants surviving compared to 80% survival of wild-type mice

hematopoietic system
• macrophage recruitment to inflamed lungs is increased
• number of resident alveolar macrophages in unchallenged mutants is increased by more than 60% percent compared to wild-type
• neutrophils isolated from bone marrow live longer than wild-type neutrophils (J:114699)
• neutrophils exhibit enhanced ruffling in response to the chemoattractant fMLP or IL-8 (J:145331)
• polarized neutrophils exhibit a considerable increase in multiple pseudopodia compared to wild-type mice (J:145331)
• neutrophils show more diffuse F-actin localization at the leading edge or pseudopodia than wild-type neutrophils (J:145331)
• fMLP-stimulated, but not PMA-stimulated, neutrophils exhibit increased and prolonged superoxide production compared to wild-type neutrophils (J:145331)
• neutrophils exhibit enhanced transwell chemotaxis toward fMLP, IL-8 or C5a (J:145331)
• neutrophils are more active and move faster than wild-type neutrophils but lack some of the directionality of wild-type neutrophils (J:145331)
• in a model of peritonitis, neutrophil recruitment at sites of inflammation is increased in mutants compared to wild-type mice (J:145331)
• in a model of bacterial pneumonia, apoptosis of lung recruited neutrophils is reduced in mutants compared to wild-type mice (J:148947)
• neutrophils exhibit enhanced bacteria-killing capacity in a model of bacterial pneumonia (J:148947)
• neutrophils have an increased phagocytic index compared to wild-type in a model of bacterial pneumonia (J:148947)
• neutrophils exhibit enhanced E.coli and zymosan-induced phagocytosis-associated superoxide production (J:148947)
• in a bacterial pneumonia model in which mutants are intratracheally infected with E.coli to induce lung inflammation, mutants exhibit an increase in bacteria-induced neutrophil recruitment compared to controls
• mutants treated with the chemotherapeutic drug, cyclophosphamide, to induce neutropenia, exhibit fewer neutrophils in the lungs than untreated mutants, but more neutrophils than drug treated wild-type mice

homeostasis/metabolism
• increased neutrophil recruitment to lungs leads to pulmonary edema formation and increased protein accumulation
• increase in cytokine/chemokine concentrations in inflamed lungs of E.coli infected mutants due to increased numbers of resident alveolar macrophages and not due to enhanced capability of macrophages to produce cytokines or chemokines

mortality/aging
• mutants made neutropenic with the chemotherapeutic drug, cyclophosphamide, exhibit decreased mortality after E.coli challenge compared to wild-type mice due to enhanced neutrophil accumulation in the lungs (50% survival for mutants compared to 7% survival for wild-type mice)
• mutants exhibit an increase in pneumonia-associated death rate compared to wild-type mice, with only 50% of mutants surviving compared to 80% survival of wild-type mice

respiratory system
• number of resident alveolar macrophages in unchallenged mutants is increased by more than 60% percent compared to wild-type
• increased neutrophil recruitment to lungs leads to pulmonary edema formation and increased protein accumulation
• mutants develop more severe lung inflammation in response to bacterial pneumonia than controls

cellular
• macrophage recruitment to inflamed lungs is increased




Genotype
MGI:4441491
cn58
Allelic
Composition
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (7 available); any Kras mutation (36 available)
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the maximum survival is 24 days

respiratory system
• lung weight is 10-fold higher than that in control mice at 3 weeks old

neoplasm




Genotype
MGI:3801426
cn59
Allelic
Composition
Mcl1tm1Ywh/Mcl1tm1Ywh
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lyz2tm1(cre)Ifo mutation (9 available); any Lyz2 mutation (14 available)
Mcl1tm1Ywh mutation (0 available); any Mcl1 mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• despite reduced neutrophil numbers and recruitment, the number of monocytes, recruitment of macrophages during peritonitis and macrophage survival and cytokine production after Toll-like receptor stimulation are normal
• in the blood, spleen and bone marrow
• the number of Mac-1+Gr1+ granulocytes is decreased in the bone marrow as well as decreased 80% in peripheral blood and 86% in spleen compared to in wild-type mice
• the number of neutrophils is reduced by 80% compared to in wild-type mice due to increased apoptosis of neutrophils
• however, mice that do not exhibit proper cre-mediated deletion survive
• apoptosis of neutrophils is enhanced
• however, mice that do not exhibit proper cre-mediated deletion survive
• mice exhibit an 80% decrease in neutrophils recruited to peritoneal cells treated with thioglycollate to induce peritonitis compared to similarly treated wild-type mice

hematopoietic system
• in the blood, spleen and bone marrow
• the number of Mac-1+Gr1+ granulocytes is decreased in the bone marrow as well as decreased 80% in peripheral blood and 86% in spleen compared to in wild-type mice
• the number of neutrophils is reduced by 80% compared to in wild-type mice due to increased apoptosis of neutrophils
• however, mice that do not exhibit proper cre-mediated deletion survive
• apoptosis of neutrophils is enhanced
• however, mice that do not exhibit proper cre-mediated deletion survive
• mice exhibit an 80% decrease in neutrophils recruited to peritoneal cells treated with thioglycollate to induce peritonitis compared to similarly treated wild-type mice




Genotype
MGI:4441492
cn60
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N