Phenotypes associated with this allele

• Allele Symbol: Ccl2^tm1Rol
• Allele Name: targeted mutation 1, Barrett J Rollins
• Allele ID: MGI:2175911
• Summary: 17 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ccl2^tm1Rol/Ccl2^tm1Rol	(129S4/SvJae x C57BL/6)F1	MGI:4418564
hm2	Ccl2^tm1Rol/Ccl2^tm1Rol	B6.129S4-Ccl2^tm1Rol	MGI:3815114
hm3	Ccl2^tm1Rol/Ccl2^tm1Rol	B6.129S4-Ccl2^tm1Rol/J	MGI:4418677
hm4	Ccl2^tm1Rol/Ccl2^tm1Rol	involves: 129S4/SvJae	MGI:3712663
hm5	Ccl2^tm1Rol/Ccl2^tm1Rol	involves: 129S4/SvJae * 129X1/SvJ * C57BL/6	MGI:2660685
hm6	Ccl2^tm1Rol/Ccl2^tm1Rol	involves: 129S4/SvJae * C57BL/6	MGI:3694966
hm7	Ccl2^tm1Rol/Ccl2^tm1Rol	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:4418574
hm8	Ccl2^tm1Rol/Ccl2^tm1Rol	SJL.129S4-Ccl2^tm1Rol	MGI:3815119
cx9	Ccl2^tm1Rol/Ccl2^tm1Rol Ccr2^tm1Mae/Ccr2^tm1Mae	B6.129-Ccr2^tm1Mae Ccl2^tm1Rol	MGI:4418654
cx10	Ccl2^tm1Rol/Ccl2^tm1Rol Cx3cr1^tm1Zm/Cx3cr1^tm1Zm	involves: 129 * 129S4/SvJae	MGI:3814819
cx11	Ccl2^tm1Rol/Ccl2^tm1Rol Cx3cr1^tm1Litt/Cx3cr1^tm1Litt	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:5527432
cx12	Ccl2^tm1Rol/Ccl2^+ Mpz^tm1Msch/Mpz^+	involves: 129S4/SvJae * 129S7/SvEvBrd	MGI:4418726
cx13	Ccl2^tm1Rol/Ccl2^tm1Rol Mpz^tm1Msch/Mpz^+	involves: 129S4/SvJae * 129S7/SvEvBrd	MGI:4418725
cx14	Ccl2^tm1Rol/Ccl2^tm1Rol Ldlr^tm1Her/Ldlr^tm1Her	involves: 129S4/SvJae * 129S7/SvEvBrd * C57BL/6	MGI:4418562
cx15	Ccl2^tm1Rol/Ccl2^tm1Rol Tg(Ccr2-GFP)8Pam/0	involves: 129S4/SvJae * C57BL/6J	MGI:4950285
cx16	Ccl2^tm1Rol/Ccl2^+ Tg(PMP22)C61Clh/0	involves: 129S4/SvJae * C57BL/6J * CBA/Ca	MGI:4819493
cx17	Ccl2^tm1Rol/Ccl2^tm1Rol Tg(PMP22)C61Clh/0	involves: 129S4/SvJae * C57BL/6J * CBA/Ca	MGI:4819494

Genotype
MGI:4418564

hm1

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: (129S4/SvJae x C57BL/6)F1

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

hematopoietic system

decreased macrophage cell number ( J:119615 )

• following induction of nephrotoxic serum nephritis, mice exhibit reduced macrophage accumulation in the interstitium and adjacent to damaged tubules compared with similarly treated wild-type mice

• however, the number macrophages in the glomeruli is normal following induction of nephrotoxic serum nephritis

homeostasis/metabolism

abnormal response to injury ( J:119615 )

• following induction of nephrotoxic serum nephritis, mice exhibit reduced tubule damage and macrophage accumulation compared with similarly treated wild-type mice

• however, mice exhibit normal IgG/C3 deposition, proteinuria, glomerular macrophage accumulation, and glomerular damage following induction of nephrotoxic serum nephritis

immune system

decreased macrophage cell number ( J:119615 )

• following induction of nephrotoxic serum nephritis, mice exhibit reduced macrophage accumulation in the interstitium and adjacent to damaged tubules compared with similarly treated wild-type mice

• however, the number macrophages in the glomeruli is normal following induction of nephrotoxic serum nephritis

Genotype
MGI:3815114

hm2

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: B6.129S4-Ccl2^tm1Rol

Ccl2^tm1Rol/Ccl2^tm1Rol mice with experimental autoimmune encephalomyelitis show fewer inflammatory infiltrates in the spinal cord

immune system

abnormal macrophage chemotaxis ( J:109290 )

• the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice

• the total number of macrophages recruited is normal

impaired macrophage chemotaxis ( J:68145 , J:118606 , J:151874 )

• mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE (J:68145)

• initially following femoral artery excision (J:118606)

• only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls (J:151874)

increased neutrophil cell number ( J:118606 )

• 1 and 3 days after femoral artery excision, mice exhibit an earlier increase in neutrophil accumulation (measured by MPO activity) than in similarly treated wild-type mice

increased CD4-positive, alpha-beta T cell number ( J:68145 )

• in an EAE model, mutants show an increase in proportion of CD4+ cells and reduction in CD11b+CD4- in the CNS leukocyte infiltrates compared to wild-type, although total numbers of T cells are not different

increased osteoclast cell number ( J:109290 )

• at P5 during tooth eruption

• peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice

decreased leukocyte cell number ( J:68145 )

• numbers of leukocytes isolated from CNS tissue during EAE attacks are about 1/3 of those from wild type mice with comparable EAE severity

decreased macrophage cell number ( J:147328 )

• age-dependent accumulation of macrophages in the choroids is less than in wild-type mice

abnormal neutrophil physiology ( J:151874 )

• the number of neutrophils recruited to the peritoneum in an induced peritonitis model is almost double that controls

increased IgG level ( J:147328 )

• at 16 months, IgG is present in the retinal pigmented epithelium or choroids unlike in wild-type mice

• IgG light chain deposition in the retinal pigmented epithelium accumulates with age unlike in wild-type mice

increased IgG1 level ( J:68145 )

• significantly higher levels of anti-MOG35-55 IgG1 antibodies are seen in mutants compared to wild-type

abnormal chemokine level ( J:118606 , J:151874 )

• 1 day after femoral artery excision, muscles accumulate more chemoattractants (KC and MIP-2) than in similarly treated wild-type mice (J:118606)

• in thioglycollate- or zymosan- induced peritonitis models, no Ccl2 is detected while reduce levels of Ccl7 are present in peritoneal fluid (J:151874)

abnormal cytokine secretion ( J:68145 )

• MOG35-55-specific Th1 cytokine responses are diminished in mutants

abnormal chemokine secretion ( J:151874 )

• there is no Ccl2 (MCP-1) secretion by peritoneal macrophages activated in vitro compared to controls

• secretion of Ccl7 (MCP-3) and Ccl12 (MCP-5) is also dramatically reduced by these activated macrophages

decreased interferon-gamma secretion ( J:68145 )

• mutants exhibit reduced production of IFN-gamma in response to MOG35-55 induced EAE

increased interleukin-10 secretion ( J:68145 )

• mutants exhibit enhanced secretion of IL-10 in response to MOG35-55 induced EAE

decreased susceptibility to experimental autoimmune encephalomyelitis ( J:68145 )

• homozygotes are resistant to active experimental autoimmune encephalomyelitis (EAE) induction with MOG35-55, with delayed onset of disease, reduced inflammatory reaction including impaired recruitment of macrophages to the central nervous system (CNS), and faster and complete recovery

• adoptive transfer of primed T cells from wild-type mice to naive homozygous mutant recipients does not mediate clinical EAE, however wild-type mice receiving mutant T cells do develop clinical EAE

vision/eye

retina photoreceptor degeneration ( J:147328 )

• at 16 months

abnormal retina pigment epithelium morphology ( J:147328 )

• after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice

• at 16 months, mice exhibit attenuation of the retinal pigmented epithelium unlike in wild-type mice

retina outer nuclear layer degeneration ( J:147328 )

• at 16 months

increased susceptibility to age-related retinal degeneration ( J:147328 )

• at 16 months, mice exhibit progressive outer retinal degeneration and confluent areas of visible atrophy unlike in wild-type mice

• at 18 months, mice exhibit geographic atrophy unlike in wild-type mice

retina deposits ( J:147328 )

• after 9 months of age, mice exhibit subretinal deposits similar to drusen that increase with age unlike in wild-type mice

abnormal optic choroid morphology ( J:147328 )

• age-dependent accumulation of macrophages in the choroids is less than in wild-type mice

abnormal choriocapillaris morphology ( J:147328 )

• at 16 months, mice exhibit dilation and attenuation of the choriocapillaris unlike wild-type mice

choroidal neovascularization ( J:147328 )

• at 15 to 19 months, mice exhibit intrachoroidal neovascularization with angiographic leakage unlike wild-type mice

• after 18 months, 4 of 15 mice exhibit choroidal neovascularization with angiographic leakage unlike in wild-type mice

• between 18 and 27 months, neovasculatization breaches the Bruch membrane and causes retinal pigmented epithelium and photoreceptor disruptions unlike in wild-type mice

abnormal Bruch membrane morphology ( J:147328 )

• the Bruch membrane is thickened compared to in wild-type mice after 9 months of age

• at 20 months, the outer Bruch membrane is breached by choriocapillary processes unlike in wild-type mice

behavior/neurological

alcohol aversion ( J:102583 )

♀ • in female mice

alcohol preference ( J:102583 )

• male mice exhibit a greater ethanol preference compared with wild-type (in post hoc analysis) mice, Ccr2^tm1Mae homozygotes, and Ccl2^tm1Rol Ccr2^tm1Mae double homozygotes

• female mice exhibit a greater ethanol preference compared with Ccl2^tm1Rol Ccr2^tm1Mae double homozygotes and Ccr2^tm1Mae homozygotes

decreased alcohol consumption ( J:102583 )

♀ • in female mice compared with wild-type mice and Ccr2^tm1Mae homozygotes

abnormal conditioned taste aversion behavior ( J:102583 )

• mice exhibit a stronger response to ethanol in an ethanol-induced conditioned taste aversion test compared with similarly treated wild-type mice

• however, saccharin consumption is normal

increased fluid intake ( J:102583 )

• mice exhibit increased drinking of an ethanol solution compared with Ccl2^tm1Rol Ccr2^tm1Mae double homozygotes and Ccr2^tm1Mae homozygotes

• mice exhibit increased drinking of a quinine solution compared with wild-type mice

increased alcohol consumption ( J:102583 )

• male mice consume more ethanol than wild-type (in post hoc analysis) mice and Ccl2^tm1Rol Ccr2^tm1Mae double homozygotes

• female mice consume more ethanol than Ccl2^tm1Rol Ccr2^tm1Mae double homozygotes

impaired righting response ( J:102583 )

• mice exhibit longer duration of ethanol-induced loss of righting response compared with similarly treated wild-type mice

cardiovascular system

abnormal choriocapillaris morphology ( J:147328 )

• at 16 months, mice exhibit dilation and attenuation of the choriocapillaris unlike wild-type mice

choroidal neovascularization ( J:147328 )

• at 15 to 19 months, mice exhibit intrachoroidal neovascularization with angiographic leakage unlike wild-type mice

• after 18 months, 4 of 15 mice exhibit choroidal neovascularization with angiographic leakage unlike in wild-type mice

• between 18 and 27 months, neovasculatization breaches the Bruch membrane and causes retinal pigmented epithelium and photoreceptor disruptions unlike in wild-type mice

abnormal blood circulation ( J:118606 )

• following femoral artery excision, mice exhibit a delay in the restoration of perfusion compared with similarly treated wild-type mice

nervous system

retina photoreceptor degeneration ( J:147328 )

• at 16 months

pigmentation

abnormal retina pigment epithelium morphology ( J:147328 )

• after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice

• at 16 months, mice exhibit attenuation of the retinal pigmented epithelium unlike in wild-type mice

lipofuscinosis ( J:147328 )

• after 9 months of age, lipofuscin granules are observed in the swollen and vacuolated retinal pigmented epithelial cells unlike in wild-type mice

hematopoietic system

abnormal macrophage chemotaxis ( J:109290 )

• the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice

• the total number of macrophages recruited is normal

impaired macrophage chemotaxis ( J:68145 , J:118606 , J:151874 )

• mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE (J:68145)

• initially following femoral artery excision (J:118606)

• only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls (J:151874)

increased neutrophil cell number ( J:118606 )

• 1 and 3 days after femoral artery excision, mice exhibit an earlier increase in neutrophil accumulation (measured by MPO activity) than in similarly treated wild-type mice

increased CD4-positive, alpha-beta T cell number ( J:68145 )

• in an EAE model, mutants show an increase in proportion of CD4+ cells and reduction in CD11b+CD4- in the CNS leukocyte infiltrates compared to wild-type, although total numbers of T cells are not different

increased osteoclast cell number ( J:109290 )

• at P5 during tooth eruption

• peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice

decreased leukocyte cell number ( J:68145 )

• numbers of leukocytes isolated from CNS tissue during EAE attacks are about 1/3 of those from wild type mice with comparable EAE severity

decreased macrophage cell number ( J:147328 )

• age-dependent accumulation of macrophages in the choroids is less than in wild-type mice

abnormal neutrophil physiology ( J:151874 )

• the number of neutrophils recruited to the peritoneum in an induced peritonitis model is almost double that controls

increased IgG level ( J:147328 )

• at 16 months, IgG is present in the retinal pigmented epithelium or choroids unlike in wild-type mice

• IgG light chain deposition in the retinal pigmented epithelium accumulates with age unlike in wild-type mice

increased IgG1 level ( J:68145 )

• significantly higher levels of anti-MOG35-55 IgG1 antibodies are seen in mutants compared to wild-type

homeostasis/metabolism

abnormal chemokine level ( J:118606 , J:151874 )

• 1 day after femoral artery excision, muscles accumulate more chemoattractants (KC and MIP-2) than in similarly treated wild-type mice (J:118606)

• in thioglycollate- or zymosan- induced peritonitis models, no Ccl2 is detected while reduce levels of Ccl7 are present in peritoneal fluid (J:151874)

decreased physiological sensitivity to xenobiotic ( J:110695 )

• bleomycin-treated mice fail to exhibit skin fibrosis with normal collagen fibrils and few infiltrating macrophages and neutrophils unlike similarly treated wild-type mice

abnormal response to injury ( J:118606 )

• following femoral artery excision, mice exhibit a delay in the restoration of perfusion, extended period of increased ischemic muscle weight at day 1 and 7, earlier increase in neutrophil accumulation (measured by MPO activity) at day 1 and 3, increased chemoattractants (KC and MIP-2) levels at day 1, decreased accumulation of inflammatory infiltrate at day 3, delayed macrophage recruitment, large regions of necrotic muscle, increased adipocyte accumulation in the muscle, and impaired muscle regeneration compared with similarly treated wild-type mice

craniofacial

premature tooth eruption ( J:109290 )

• tooth eruption begins at P14 instead of P16 as in wild-type mice

• from P16 to P18, mice exhibit a 31-fold increase in erupted cusps compared with wild-type mice

skeleton

premature tooth eruption ( J:109290 )

• tooth eruption begins at P14 instead of P16 as in wild-type mice

• from P16 to P18, mice exhibit a 31-fold increase in erupted cusps compared with wild-type mice

increased osteoclast cell number ( J:109290 )

• at P5 during tooth eruption

• peak osteoclast accumulation occurs at P5 instead of at P9 as in wild-type mice

muscle

increased muscle weight ( J:118606 )

• after 1 and 7 days, mice subjected to femoral artery excision exhibit an extended period of increased ischemic muscle weight compared with similarly treated wild-type mice

abnormal skeletal muscle morphology ( J:118606 )

• following femoral artery excision, muscles accumulate more adipocytes than in similarly treated wild-type mice

skeletal muscle necrosis ( J:118606 )

• following femoral artery excision

impaired skeletal muscle regeneration ( J:118606 )

• muscle regeneration, as measured by LDH and fiber size, is impaired following femoral artery excision

cellular

skeletal muscle necrosis ( J:118606 )

• following femoral artery excision

abnormal macrophage chemotaxis ( J:109290 )

• the timing of macrophage recruitment during tooth eruption is different than in wild-type mice with peak numbers occurring earlier than in wild-type mice

• the total number of macrophages recruited is normal

impaired macrophage chemotaxis ( J:68145 , J:118606 , J:151874 )

• mutants show impaired macrophage recruitment to the CNS after MOG35-55 induced EAE (J:68145)

• initially following femoral artery excision (J:118606)

• only half the number of macrophages are recruited to the peritoneum in an induced peritonitis model as occurs in wild-type controls (J:151874)

growth/size/body

premature tooth eruption ( J:109290 )

• tooth eruption begins at P14 instead of P16 as in wild-type mice

• from P16 to P18, mice exhibit a 31-fold increase in erupted cusps compared with wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
age related macular degeneration		DOID:10871	OMIM:PS603075	J:147328

Genotype
MGI:4418677

hm3

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: B6.129S4-Ccl2^tm1Rol/J

homeostasis/metabolism

decreased susceptibility to neuronal excitotoxicity ( J:141739 )

• mice treated with kainate acid exhibit decreased microglial accumulation and reduced neurodegeneration in the CA1 and CA3 pyramidal neurons compared with similarly treated wild-type mice

increased susceptibility to diet-induced obesity ( J:126512 )

• when fed a high fat diet, mice exhibit a mildly enhanced weight gain compared with similarly treated wild-type mice

• at 18 to 34 weeks, mice fed a high fat diet exhibit a 13% increase in body weight compared with similarly treated wild-type mice

increased circulating leptin level ( J:126512 )

• when fed a high fat diet

decreased circulating free fatty acids level ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

abnormal glucose homeostasis ( J:126512 )

increased circulating glucose level ( J:126512 )

• mild in fasting mice regardless of diet

decreased circulating insulin level ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

increased circulating insulin level ( J:126512 )

• when fed a high fat diet

abnormal gluconeogenesis ( J:110277 )

• during hyperinsulinemic-euglycemic clamp analysis, mice fed a high fat diet exhibit a 3-fold increase in basal and clamp hepatic glucose production compared with similarly treated wild-type mice

impaired glucose tolerance ( J:126512 )

• at 14 and 27 weeks regardless of diet

improved glucose tolerance ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

increased insulin sensitivity ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

decreased adiponectin level ( J:126512 )

• regardless of diet

increased adiponectin level ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

behavior/neurological

abnormal touch/ nociception ( J:326871 )

• mice fail to exhibit nociceptive hypersensitivity to mechanical, heat, and cold stimuli induced by injection of an adenovirus overexpressing Gm34583 unlike control mice

adipose tissue

decreased fat cell size ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

abnormal epididymal fat pad morphology ( J:110277 )

• when fed a high fat diet, macrophage infiltration of the epididymal fat pad is reduced compared to in similarly treated wild-type mice

abnormal gonadal fat pad morphology ( J:126512 )

• mice fed a high fat diet exhibit a mild increase in macrophage infiltration of adipose tissue compared with similarly treated wild-type mice

• however, macrophage numbers in subcutaneous fat when fed a standard diet is normal

increased total fat pad weight ( J:126512 )

• when fed a high fat diet

increased percent body fat/body weight ( J:126512 )

• 15% in mice fed a high fat diet compared with similarly treated wild-type mice

liver/biliary system

decreased susceptibility to diet-induced hepatic steatosis ( J:110277 )

• when mice are fed a high fat diet compared with similarly treated wild-type mice

growth/size/body

decreased body weight ( J:126512 )

• slightly when mice are fed a standard diet

increased susceptibility to diet-induced obesity ( J:126512 )

• when fed a high fat diet, mice exhibit a mildly enhanced weight gain compared with similarly treated wild-type mice

• at 18 to 34 weeks, mice fed a high fat diet exhibit a 13% increase in body weight compared with similarly treated wild-type mice

nervous system

abnormal microglial cell physiology ( J:141739 )

• mice treated with kainate acid exhibit decreased microglial accumulation compared with similarly treated wild-type mice

abnormal action potential ( J:326871 )

• small, medium, and large neurons from mice injected with an adenovirus overexpressing Gm34583 fail to exhibit increases in the number of action potentials evoked by injected currents unlike control neurons

abnormal neuron physiology ( J:326871 )

• small, medium, and large neurons from mice injected with an adenovirus overexpressing Gm34583 fail to exhibit depolarization unlike control neurons

• small and medium, but not large, neurons from mice injected with an adenovirus overexpressing Gm34583 fail to exhibit an increase in the frequency of spontaneous activity unlike control neurons

decreased susceptibility to neuronal excitotoxicity ( J:141739 )

• mice treated with kainate acid exhibit decreased microglial accumulation and reduced neurodegeneration in the CA1 and CA3 pyramidal neurons compared with similarly treated wild-type mice

immune system

abnormal microglial cell physiology ( J:141739 )

• mice treated with kainate acid exhibit decreased microglial accumulation compared with similarly treated wild-type mice

cellular

decreased susceptibility to neuronal excitotoxicity ( J:141739 )

• mice treated with kainate acid exhibit decreased microglial accumulation and reduced neurodegeneration in the CA1 and CA3 pyramidal neurons compared with similarly treated wild-type mice

hematopoietic system

abnormal microglial cell physiology ( J:141739 )

• mice treated with kainate acid exhibit decreased microglial accumulation compared with similarly treated wild-type mice

Genotype
MGI:3712663

hm4

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: involves: 129S4/SvJae

mortality/aging

increased susceptibility to infection induced morbidity/mortality ( J:155025 )

• following infection with the parasite T. cruzi, mice exhibit earlier and increased lethality compared with similarly treated wild-type mice

immune system

decreased lymphocyte cell number ( J:147697 )

• in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice

decreased macrophage cell number ( J:147697 )

• in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice

abnormal monocyte morphology ( J:121281 )

• 7/4^bri and 7/4^dim cells are decreased in blood by 50%

• intraperitoneal thioglycollate challenge leads to an increase in 7/4^bri cells

abnormal macrophage physiology ( J:155025 )

• activated macrophage clear trypomastigotes less efficiently than wild-type cells

impaired macrophage chemotaxis ( J:147697 )

• to the lungs of bleomycin-treated mice compared with similarly treated wild-type mice

increased circulating interferon-gamma level ( J:155025 )

• following infection with T. cruzi

increased circulating interleukin-10 level ( J:155025 )

• following infection with T. cruzi

increased circulating tumor necrosis factor level ( J:155025 )

• following infection with T. cruzi

decreased inflammatory response ( J:155025 )

• following infection with T. cruzi, mice exhibit decreased focal infiltration of leukocytes (recruitment of activated CD8+ cells and monocytes) in the heart and liver compared with similarly treated wild-type mice

increased susceptibility to infection induced morbidity/mortality ( J:155025 )

• following infection with the parasite T. cruzi, mice exhibit earlier and increased lethality compared with similarly treated wild-type mice

increased susceptibility to parasitic infection ( J:155025 )

• mice infected with T. cruzi exhibit increased mortality; prostration, vasodilation and rough hair close to the time of death; increased plasma TNF, IFN-gamma, and IL10 levels; increased tissue parasitic burden with reduced focal leukocyte infiltration; and unlike in similarly treated wild-type mice

homeostasis/metabolism

increased circulating interferon-gamma level ( J:155025 )

• following infection with T. cruzi

increased circulating interleukin-10 level ( J:155025 )

• following infection with T. cruzi

increased circulating tumor necrosis factor level ( J:155025 )

• following infection with T. cruzi

decreased physiological sensitivity to xenobiotic ( J:147697 )

• mice are protected from bleomycin-induced lung fibrosis with fewer recruited alveolar macrophages and lymphocytes in the lungs compared with similarly treated wild-type mice

hematopoietic system

decreased lymphocyte cell number ( J:147697 )

• in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice

decreased macrophage cell number ( J:147697 )

• in the bronchoalveolar lavage of bleomycin-treated mice compared with similarly treated wild-type mice

abnormal monocyte morphology ( J:121281 )

• 7/4^bri and 7/4^dim cells are decreased in blood by 50%

• intraperitoneal thioglycollate challenge leads to an increase in 7/4^bri cells

abnormal macrophage physiology ( J:155025 )

• activated macrophage clear trypomastigotes less efficiently than wild-type cells

impaired macrophage chemotaxis ( J:147697 )

• to the lungs of bleomycin-treated mice compared with similarly treated wild-type mice

behavior/neurological

abnormal posture ( J:155025 )

• following infection with T. cruzi, mice exhibit prostration as they near death unlike similarly treated wild-type mice

cardiovascular system

increased vasodilation ( J:155025 )

• following infection with T. cruzi as mice near death

muscle

increased vasodilation ( J:155025 )

• following infection with T. cruzi as mice near death

cellular

impaired macrophage chemotaxis ( J:147697 )

• to the lungs of bleomycin-treated mice compared with similarly treated wild-type mice

Genotype
MGI:2660685

hm5

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: involves: 129S4/SvJae * 129X1/SvJ * C57BL/6

immune system

impaired macrophage chemotaxis ( J:45920 )

• impaired macrophage recruitment following intraperitoneal thioglycollate injection

abnormal monocyte morphology ( J:45920 )

• mutants are unable to recruit monocytes 72 hours after intraperitoneal thioglycollate administration despite normal numbers of circulating leukocytes and macrophages

decreased susceptibility to type IV hypersensitivity reaction ( J:45920 )

• accumulation of F4/80+ monocytes in delayed-type hypersensitivity lesions is impaired, although the swelling response is normal

• development of secondary pulmonary granulomata in response to Schistosoma mansoni eggs in blunted

decreased interferon-gamma secretion ( J:45920 )

• IFN-gamma secretion is 59% lower in mutant splenocytes

decreased interleukin-4 secretion ( J:45920 )

• IL-4 production is reduced in splenocytes

decreased interleukin-5 secretion ( J:45920 )

• IL-5 production is reduced in splenocytes

hematopoietic system

impaired macrophage chemotaxis ( J:45920 )

• impaired macrophage recruitment following intraperitoneal thioglycollate injection

abnormal monocyte morphology ( J:45920 )

• mutants are unable to recruit monocytes 72 hours after intraperitoneal thioglycollate administration despite normal numbers of circulating leukocytes and macrophages

cellular

impaired macrophage chemotaxis ( J:45920 )

• impaired macrophage recruitment following intraperitoneal thioglycollate injection

Genotype
MGI:3694966

hm6

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:116878 )

• DNBS-treated mice do not exhibit an increase in mortality compared with similarly treated wild-type mice

cardiovascular system

abnormal physiological neovascularization ( J:107646 )

• ischemic capillary density relative to nonischemic density 30% lower than in controls

• poor recovery of blood flow after ischemia

abnormal heart left ventricle morphology ( J:108533 )

• following myocardial infarction, mice exhibit lower left ventricle end diastolic diameter compared with similarly treated wild-type mice

abnormal response to cardiac infarction ( J:108533 )

• following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice

• following myocardial infarction, mice exhibit persistence of dead cardiomyocytes and delayed replacement with granulation compared with similarly treated wild-type mice

• following myocardial infarction, mice exhibit decreased myofibroblast infiltration 3 days after reperfusion compared with similarly treated wild-type mice

• following myocardial infarction, mice exhibit lower left ventricle end diastolic diameter compared with similarly treated wild-type mice

• however, mice exhibit normal macrophage density, infarct size, and angiogenesis following myocardial infarction

immune system

abnormal macrophage chemotaxis ( J:116878 )

• in colonic tissue following DNBS treatment

impaired macrophage chemotaxis ( J:108533 )

• following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice

• however, macrophage density is normal 3 to 7 days following myocardial infarction

decreased susceptibility to induced colitis ( J:116878 )

• DNBS-treated mice exhibit reduced mucosal damage; less thickening of the colonic wall; less goblet cell depletion; fewer adhesions; reduced macrophage and CD3+ T cell infiltration; reduced IL1beta, IL12p40, and ConA-stimulated production; reduced numbers of 5-HT-expressing enterochromaffin cells, and no increase in mortality compared with similarly treated wild-type mice

abnormal T cell physiology ( J:116878 )

• following DNBS treatment, infiltration of CD3+ T cells in colonic tissue is decreased compared to in wild-type mice

decreased interferon-gamma secretion ( J:116878 )

• in ConA-treated splenic cells of DNBS-treated mice

decreased interleukin-1 beta secretion ( J:116878 )

• in colonic tissue following DNBS treatment

decreased interleukin-12b secretion ( J:116878 )

• in colonic tissue following DNBS treatment

neoplasm

decreased incidence of tumors by chemical induction ( J:56068 )

• DMBA and TPA-treated mice exhibit 50% fewer skin tumors than similarly treated wild-type mice

homeostasis/metabolism

abnormal response to cardiac infarction ( J:108533 )

• following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice

• following myocardial infarction, mice exhibit persistence of dead cardiomyocytes and delayed replacement with granulation compared with similarly treated wild-type mice

• following myocardial infarction, mice exhibit decreased myofibroblast infiltration 3 days after reperfusion compared with similarly treated wild-type mice

• following myocardial infarction, mice exhibit lower left ventricle end diastolic diameter compared with similarly treated wild-type mice

• however, mice exhibit normal macrophage density, infarct size, and angiogenesis following myocardial infarction

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:116878 )

• DNBS-treated mice do not exhibit an increase in mortality compared with similarly treated wild-type mice

decreased incidence of tumors by chemical induction ( J:56068 )

• DMBA and TPA-treated mice exhibit 50% fewer skin tumors than similarly treated wild-type mice

digestive/alimentary system

decreased susceptibility to induced colitis ( J:116878 )

• DNBS-treated mice exhibit reduced mucosal damage; less thickening of the colonic wall; less goblet cell depletion; fewer adhesions; reduced macrophage and CD3+ T cell infiltration; reduced IL1beta, IL12p40, and ConA-stimulated production; reduced numbers of 5-HT-expressing enterochromaffin cells, and no increase in mortality compared with similarly treated wild-type mice

cellular

abnormal macrophage chemotaxis ( J:116878 )

• in colonic tissue following DNBS treatment

impaired macrophage chemotaxis ( J:108533 )

• following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice

• however, macrophage density is normal 3 to 7 days following myocardial infarction

hematopoietic system

abnormal macrophage chemotaxis ( J:116878 )

• in colonic tissue following DNBS treatment

impaired macrophage chemotaxis ( J:108533 )

• following myocardial infarction, mice exhibit impaired macrophage recruitment with delayed peak macrophage numbers compared with similarly treated wild-type mice

• however, macrophage density is normal 3 to 7 days following myocardial infarction

abnormal T cell physiology ( J:116878 )

• following DNBS treatment, infiltration of CD3+ T cells in colonic tissue is decreased compared to in wild-type mice

Genotype
MGI:4418574

hm7

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

homeostasis/metabolism

delayed wound healing ( J:70862 )

• at day 3 following injury, re-epithelialization is delayed with decreased vascular density at the injury compared to in similarly treated wild-type mice

• complete wound healing takes twice as long as in wild-type mice

• however, macrophage accumulation at the site of injury is normal

cardiovascular system

decreased angiogenesis ( J:70862 )

• during wound healing

Genotype
MGI:3815119

hm8

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol
• Genetic Background: SJL.129S4-Ccl2^tm1Rol

immune system

decreased susceptibility to experimental autoimmune encephalomyelitis ( J:68145 )

• homozygotes exhibit attenuated severity of PLP-induced EAE and reduced number of relapses compared to wild-type

Genotype
MGI:4418654

cx9

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Ccr2^tm1Mae/Ccr2^tm1Mae
• Genetic Background: B6.129-Ccr2^tm1Mae Ccl2^tm1Rol

behavior/neurological

alcohol aversion ( J:102583 )

• compared to in Ccl2^tm1Rol homozygotes

alcohol preference ( J:102583 )

• compared to in Ccr2^tm1Mae homozygotes

decreased alcohol consumption ( J:102583 )

• compared to in Ccl2^tm1Rol or Ccr2^tm1Mae homozygotes

Genotype
MGI:3814819

cx10

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Cx3cr1^tm1Zm/Cx3cr1^tm1Zm
• Genetic Background: involves: 129 * 129S4/SvJae

vision/eye

choroidal neovascularization ( J:126935 )

• beginning as early as 12 weeks of age,15% of mice exhibit neovascularization of the choroid unlike in wild-type mice

• choroidal neovascular vessels that penetrate Bruch membrane and enter the outer retinal layers are surrounded by hyperplastic retinal pigmented epithelium cells or atrophic retinal pigmented epithelium areas

abnormal retina morphology ( J:126935 )

• microglial infiltrates are observed in retinal lesions

disorganized photoreceptor outer segment ( J:126935 )

retina photoreceptor degeneration ( J:126935 )

• severity increases with age

abnormal retina pigment epithelium morphology ( J:126935 )

• unlike in wild-type mice, vacuolation of the retinal pigmented epithelium (RPE) is observed

• mice exhibit a reduction in melanosomes and an increase in lipofuscin in the RPE unlike in wild-type mice

abnormal retina pigmentation ( J:126935 )

• unlike in wild-type mice, local hypopigmentation of the retina is observed

retina pigment epithelium atrophy ( J:126935 )

• in some areas with severity increasing with age

retina pigment epithelium hyperplasia ( J:126935 )

• in some areas

retina deposits ( J:126935 )

• by 6 to 9 weeks, mice exhibit drusen-like lesions with heterogeneous, round or domed-shaped, soft-bordered yellowish deposits within the subretina not observed in wild-type mice

• retinal depositions enlarge or flatten and become confluent with age

abnormal Bruch membrane morphology ( J:126935 )

• beginning at 8 weeks of age, mice exhibit focal thickening in the Bruch membrane compared to wild-type mice

reproductive system

decreased litter size ( J:126935 )

• average litter size is half of wild-type

nervous system

disorganized photoreceptor outer segment ( J:126935 )

retina photoreceptor degeneration ( J:126935 )

• severity increases with age

pigmentation

variable depigmentation ( J:126935 )

• 20% of mice exhibit patchy skin depigmentation on the face and upper extremities

abnormal retina pigment epithelium morphology ( J:126935 )

• unlike in wild-type mice, vacuolation of the retinal pigmented epithelium (RPE) is observed

• mice exhibit a reduction in melanosomes and an increase in lipofuscin in the RPE unlike in wild-type mice

abnormal retina pigmentation ( J:126935 )

• unlike in wild-type mice, local hypopigmentation of the retina is observed

retina pigment epithelium atrophy ( J:126935 )

• in some areas with severity increasing with age

retina pigment epithelium hyperplasia ( J:126935 )

• in some areas

cardiovascular system

choroidal neovascularization ( J:126935 )

• beginning as early as 12 weeks of age,15% of mice exhibit neovascularization of the choroid unlike in wild-type mice

• choroidal neovascular vessels that penetrate Bruch membrane and enter the outer retinal layers are surrounded by hyperplastic retinal pigmented epithelium cells or atrophic retinal pigmented epithelium areas

integument

variable depigmentation ( J:126935 )

• 20% of mice exhibit patchy skin depigmentation on the face and upper extremities

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
age related macular degeneration		DOID:10871	OMIM:PS603075	J:126935

Genotype
MGI:5527432

cx11

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Cx3cr1^tm1Litt/Cx3cr1^tm1Litt
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J

Retinal lesion in Ccl2^tm1Rol/Ccl2^tm1Rol Cx3cr1^tm1Litt/Cx3cr1^tm1Litt mice

vision/eye

abnormal retina morphology ( J:200877 )

• patches of yellowish/whitish fundus lesions are seen in 17-60% of 12 month old and 30-100% of 18 month old mutants

• majority of lesions are in the temporal area (upper and lower) between the optic disc and equatorial region of the retina, with variable lesion size and lesions are rarely seen in the peripheral retinal areas

• 83-100% of mutants exposed to an approximate 800 lux light 6 hours/day for 6-7 months develop patches of yellowish and whitish lesions compared to 20-25% of wild-type mice

• aged and light-treated mutant retinas exhibit mitochondrial damage, vacuolization, and photoreceptor damage

• however, choroidal neovascularization is not seen in aged or 800 lux light treated mutants and induction of choroidal neovascularization using 532 nm diode laser does not differ from that seen in wild-type mice

abnormal Muller cell morphology ( J:200877 )

• increase in Muller glial activation

abnormal amacrine cell morphology ( J:200877 )

• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting amacrine cell changes in aged mutants

abnormal photoreceptor inner segment morphology ( J:200877 )

• photoreceptor inner segment damage in aged mutants

disorganized photoreceptor outer segment ( J:200877 )

• outer segment disorientation in aged mutants

retina photoreceptor degeneration ( J:200877 )

• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting photoreceptor degeneration

abnormal retina pigmentation ( J:200877 )

• older mutants exhibit pigment loss in RPE cells

retina pigment epithelium atrophy ( J:200877 )

• 33% of 12 month old and 50% of 18 month old mutants exhibit retinal pigment epithelium (RPE) damage, showing altered cell junction, loss of hexagonal tessellation, and uneven distribution of F-actin

• older mutants exhibit multiple vacuoles in the RPE

• all mutants exhibit RPE lesions after light-treatment (800 Lux) compared to 20% of wild-type mice

increased susceptibility to age-related retinal degeneration ( J:200877 )

• mice develop age- and light-mediated retinal damage

abnormal Bruch membrane morphology ( J:200877 )

• increase in Bruch membrane thickness in aged mutants

pigmentation

abnormal retina pigmentation ( J:200877 )

• older mutants exhibit pigment loss in RPE cells

retina pigment epithelium atrophy ( J:200877 )

• 33% of 12 month old and 50% of 18 month old mutants exhibit retinal pigment epithelium (RPE) damage, showing altered cell junction, loss of hexagonal tessellation, and uneven distribution of F-actin

• older mutants exhibit multiple vacuoles in the RPE

• all mutants exhibit RPE lesions after light-treatment (800 Lux) compared to 20% of wild-type mice

nervous system

abnormal microglial cell morphology ( J:200877 )

• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas

increased microglial cell activation ( J:200877 )

• increase in microglial activation as indicated by an increase in microglial cells in the inner plexiform layer and the outer plexiform layer at 18 months of age and in chronic-light treated mutants

abnormal Muller cell morphology ( J:200877 )

• increase in Muller glial activation

abnormal amacrine cell morphology ( J:200877 )

• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting amacrine cell changes in aged mutants

abnormal photoreceptor inner segment morphology ( J:200877 )

• photoreceptor inner segment damage in aged mutants

disorganized photoreceptor outer segment ( J:200877 )

• outer segment disorientation in aged mutants

retina photoreceptor degeneration ( J:200877 )

• expression of rhodopsin, cone arrestin, and GABA are disrupted suggesting photoreceptor degeneration

hematopoietic system

abnormal microglial cell morphology ( J:200877 )

• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas

abnormal macrophage physiology ( J:200877 )

• bone marrow derived macrophages exhibit reduced phagocytic activity

increased microglial cell activation ( J:200877 )

• increase in microglial activation as indicated by an increase in microglial cells in the inner plexiform layer and the outer plexiform layer at 18 months of age and in chronic-light treated mutants

immune system

abnormal microglial cell morphology ( J:200877 )

• microglial cells in aged and chronic light-treated mice show shorter and larger dendrites and larger somas

abnormal macrophage physiology ( J:200877 )

• bone marrow derived macrophages exhibit reduced phagocytic activity

increased microglial cell activation ( J:200877 )

• increase in microglial activation as indicated by an increase in microglial cells in the inner plexiform layer and the outer plexiform layer at 18 months of age and in chronic-light treated mutants

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
age related macular degeneration		DOID:10871	OMIM:PS603075	J:200877

Genotype
MGI:4418726

cx12

• Allelic Composition: Ccl2^tm1Rol/Ccl2⁺; Mpz^tm1Msch/Mpz⁺
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd

nervous system

neuron degeneration ( J:133028 )

• at 12 months, mice exhibit demyelinating neuropathy unlike wild-type mice that is not as severe as in Mpz^tm1Msch heterozygotes or Ccl2^tm1Rol/Ccl2⁺ Mpz^tm1Msch/Mpz⁺ mice

demyelination ( J:133028 )

• at 12 months but not as severe as in Mpz^tm1Msch heterozygotes or Ccl2^tm1Rol/Ccl2⁺ Mpz^tm1Msch/Mpz⁺ mice

immune system

abnormal macrophage derived foam cell morphology ( J:133028 )

• at 12 months, the number of foam macrophages in the quadriceps nerve is decreased compared to in Ccl2^tm1Rol/Ccl2^tm1Rol Mpz^tm1Msch/Mpz⁺ mice

decreased macrophage cell number ( J:133028 )

• at 6 months, the number of macrophages in the quadriceps nerves is decreased compared to in Mpz^tm1Msch heterozygotes

• at 12 months, the number of macrophages in the quadriceps nerve is decreased compared to in Mpz^tm1Msch heterozygotes and Ccl2^tm1Rol/Ccl2^tm1Rol Mpz^tm1Msch/Mpz⁺ mice

hematopoietic system

abnormal macrophage derived foam cell morphology ( J:133028 )

• at 12 months, the number of foam macrophages in the quadriceps nerve is decreased compared to in Ccl2^tm1Rol/Ccl2^tm1Rol Mpz^tm1Msch/Mpz⁺ mice

decreased macrophage cell number ( J:133028 )

• at 6 months, the number of macrophages in the quadriceps nerves is decreased compared to in Mpz^tm1Msch heterozygotes

• at 12 months, the number of macrophages in the quadriceps nerve is decreased compared to in Mpz^tm1Msch heterozygotes and Ccl2^tm1Rol/Ccl2^tm1Rol Mpz^tm1Msch/Mpz⁺ mice

cellular

abnormal macrophage derived foam cell morphology ( J:133028 )

• at 12 months, the number of foam macrophages in the quadriceps nerve is decreased compared to in Ccl2^tm1Rol/Ccl2^tm1Rol Mpz^tm1Msch/Mpz⁺ mice

Genotype
MGI:4418725

cx13

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Mpz^tm1Msch/Mpz⁺
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd

immune system

decreased macrophage cell number ( J:133028 )

• at 6 and 12 months, the number of macrophages in the quadriceps nerve is decreased compared to in Mpz^tm1Msch heterozygotes

increased macrophage cell number ( J:133028 )

• at 12 months, the number of macrophages in the quadriceps nerve is increased 2.5-fold compared to in wild-type

abnormal cytokine level ( J:133028 )

• levels of M-CSF are increased compared to in Ccl2^tm1Rol/Ccl2⁺ Mpz^tm1Msch/Mpz⁺ mice

nervous system

neuron degeneration ( J:133028 )

• at 12 months, mice exhibit severe demyelinating neuropathy unlike wild-type mice that is more severe than in Mpz^tm1Msch heterozygotes

demyelination ( J:133028 )

• at 12 months

homeostasis/metabolism

abnormal cytokine level ( J:133028 )

• levels of M-CSF are increased compared to in Ccl2^tm1Rol/Ccl2⁺ Mpz^tm1Msch/Mpz⁺ mice

hematopoietic system

decreased macrophage cell number ( J:133028 )

• at 6 and 12 months, the number of macrophages in the quadriceps nerve is decreased compared to in Mpz^tm1Msch heterozygotes

increased macrophage cell number ( J:133028 )

• at 12 months, the number of macrophages in the quadriceps nerve is increased 2.5-fold compared to in wild-type

Genotype
MGI:4418562

cx14

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Ldlr^tm1Her/Ldlr^tm1Her
• Genetic Background: involves: 129S4/SvJae * 129S7/SvEvBrd * C57BL/6

cardiovascular system

decreased susceptibility to atherosclerosis ( J:75837 )

• when fed a high fat diet, mice exhibit decreased incidence of atherosclerosis, lipid deposition, and macrophage infiltration of aortic arches compared with similarly treated Ldlr^tm1Her homozygotes

homeostasis/metabolism

increased circulating VLDL cholesterol level ( J:75837 )

• compared to in Ldlr^tm1Her homozygotes

increased circulating triglyceride level ( J:75837 )

• compared to in Ldlr^tm1Her homozygotes

Genotype
MGI:4950285

cx15

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Tg(Ccr2-GFP)8Pam/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J

immune system

abnormal leukocyte migration ( J:171379 )

• monocytes from LPS-treated mice fail to enter the lumen of the blood vessel unlike in wild-type mice

cellular

abnormal leukocyte migration ( J:171379 )

• monocytes from LPS-treated mice fail to enter the lumen of the blood vessel unlike in wild-type mice

hematopoietic system

abnormal leukocyte migration ( J:171379 )

• monocytes from LPS-treated mice fail to enter the lumen of the blood vessel unlike in wild-type mice

Genotype
MGI:4819493

cx16

• Allelic Composition: Ccl2^tm1Rol/Ccl2⁺; Tg(PMP22)C61Clh/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * CBA/Ca

nervous system

demyelination ( J:158350 )

• myelin phenotype is improved compared to in Tg(PMP22)C61Clh mice

behavior/neurological

decreased grip strength ( J:158350 )

immune system

increased macrophage cell number ( J:158350 )

• in the femoral quadriceps nerves at 2 and 6 months of age that is not as severe Tg(PMP22)C61Clh mice

hematopoietic system

increased macrophage cell number ( J:158350 )

• in the femoral quadriceps nerves at 2 and 6 months of age that is not as severe Tg(PMP22)C61Clh mice

Genotype
MGI:4819494

cx17

• Allelic Composition: Ccl2^tm1Rol/Ccl2^tm1Rol; Tg(PMP22)C61Clh/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * CBA/Ca

nervous system

demyelination ( J:158350 )

• myelin phenotype is improved compared to in Tg(PMP22)C61Clh mice

abnormal action potential ( J:158350 )

• mice exhibit a reduced amplitude of compound action potential and a prolonged duration compared with wild-type mice but not as severely as in Tg(PMP22)C61Clh mice

decreased nerve conduction velocity ( J:158350 )

• not as severely as in Tg(PMP22)C61Clh mice

behavior/neurological

abnormal grip strength ( J:158350 )

• grip strength is improved compared to in Tg(PMP22)C61Clh mice

immune system

increased macrophage cell number ( J:158350 )

• in the femoral quadriceps nerves at 2 and 6 months of age that is not as severe Tg(PMP22)C61Clh mice

hematopoietic system

increased macrophage cell number ( J:158350 )

• in the femoral quadriceps nerves at 2 and 6 months of age that is not as severe Tg(PMP22)C61Clh mice