Phenotypes associated with this allele

• Allele Symbol: Selp^tm1Bay
• Allele Name: targeted mutation 1, Baylor College of Medicine
• Allele ID: MGI:1857244
• Summary: 14 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Selp^tm1Bay/Selp^tm1Bay	B6.129S7-Selp^tm1Bay	MGI:3835011
hm2	Selp^tm1Bay/Selp^tm1Bay	B6.129S7-Selp^tm1Bay/J	MGI:3699811
hm3	Selp^tm1Bay/Selp^tm1Bay	D1.129S7(B6J)-Selp^tm1Bay	MGI:3606585
hm4	Selp^tm1Bay/Selp^tm1Bay	either: B6.129S7-Selp^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)	MGI:3766606
hm5	Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:3766951
hm6	Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3606578
cx7	Icam1^tm1Bay/Icam1^tm1Bay Selp^tm1Bay/Selp^tm1Bay	B6.129S7-Icam1^tm1Bay Selp^tm1Bay/J	MGI:3767011
cx8	Icam1^tm1Bay/Icam1^tm1Bay Selp^tm1Bay/Selp^tm1Bay	either: B6.129S7-Selp^tm1Bay Icam1^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)	MGI:3766607
cx9	Icam1^tm1Bay/Icam1^tm1Bay Sele^tm2Alb/Sele^tm2Alb Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:3766947
cx10	Sele^tm2Alb/Sele^tm2Alb Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:3766950
cx11	Sele^tm2Alb/Sele^tm2Alb Sell^tm2Alb/Sell^tm2Alb Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6	MGI:2656301
cx12	Sele^tm2Alb/Sele^tm2Alb Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3606634
cx13	Icam1^tm1Bay/Icam1^tm1Bay Selp^tm1Bay/Selp^tm1Bay	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3606608
cx14	Fas^lpr/Fas^lpr Selp^tm1Bay/Selp^tm1Bay	MRL.Cg-Selp^tm1Bay Fas^lpr	MGI:3799723

Genotype
MGI:3835011

hm1

• Allelic Composition: Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: B6.129S7-Selp^tm1Bay

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

immune system

decreased mast cell number ( J:121083 )

• during the chronic phase of antigen exposure

decreased susceptibility to type IV hypersensitivity reaction ( J:121083 )

• chronic inflammation in response to oxazolone exposure is inhibited compared to in similarly treated wild-type mice

• however, acute inflammation in response to oxazolone exposure is normal

hematopoietic system

decreased mast cell number ( J:121083 )

• during the chronic phase of antigen exposure

Genotype
MGI:3699811

hm2

• Allelic Composition: Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: B6.129S7-Selp^tm1Bay/J

immune system

abnormal T cell physiology ( J:113536 )

• T lymphocyte migration and accumulation into cutaneous inflammatory regions induced by a combination of IFN-gamma and TNF-alpha is inhibited by about 25%, however IFN-gamma, TNF-alpha, and ConA, has no effect on T cell infiltration

hematopoietic system

abnormal T cell physiology ( J:113536 )

• T lymphocyte migration and accumulation into cutaneous inflammatory regions induced by a combination of IFN-gamma and TNF-alpha is inhibited by about 25%, however IFN-gamma, TNF-alpha, and ConA, has no effect on T cell infiltration

Genotype
MGI:3606585

hm3

• Allelic Composition: Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: D1.129S7(B6J)-Selp^tm1Bay

skeleton

increased susceptibility to induced arthritis ( J:57086 )

• accelerated incidence of induced arthritis, 23% compared to 2% of DBA/1 mice by 28 days

• increase in number of affected paws

• consistently higher arthritis severity scores as determined by inflammation, paw/digit distortion and ankylosis

• onset of arthritis occurs as early as day 14 with a median onset of 34 days

immune system

increased IgG level ( J:57086 )

• increased levels of serum IgG anti-type II collagen antibody measured in collagen immunized mice as compared to immunized DBA/1 mice

abnormal cytokine secretion ( J:57086 )

• increased levels of IL10 and IL5 measured in stimulated splenocytes

• decreased levels of IL2 and IL4 measured in stimulated splenocytes

increased susceptibility to induced arthritis ( J:57086 )

• accelerated incidence of induced arthritis, 23% compared to 2% of DBA/1 mice by 28 days

• increase in number of affected paws

• consistently higher arthritis severity scores as determined by inflammation, paw/digit distortion and ankylosis

• onset of arthritis occurs as early as day 14 with a median onset of 34 days

hematopoietic system

increased IgG level ( J:57086 )

• increased levels of serum IgG anti-type II collagen antibody measured in collagen immunized mice as compared to immunized DBA/1 mice

Genotype
MGI:3766606

hm4

• Allelic Composition: Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: either: B6.129S7-Selp^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)

hematopoietic system

abnormal leukocyte tethering or rolling ( J:31374 )

• after surgery to exteriorize cremaster muscle, mice do not display leukocyte rolling for the first hour, but a significant amount of rolling is detected after 2 hours (~8% rolling leukocyte flux)

• leukocytes show intermittent interactions with endothelium causing an increase in rolling velocity to ~129 um/second (~35 um/second in wild-type)

• treatment with Tnfa (tumor necrosis factor alpha) reduces rolling velocity to ~5 um/second

increased leukocyte cell number ( J:31374 )

• systemic leukocyte counts are ~9800/ul (~61% neutrophils, ~37% lymphocytes) compared to wild-type counts of ~5660/ul (53% neutrophils, 46% lymphocytes)

immune system

abnormal leukocyte tethering or rolling ( J:31374 )

• after surgery to exteriorize cremaster muscle, mice do not display leukocyte rolling for the first hour, but a significant amount of rolling is detected after 2 hours (~8% rolling leukocyte flux)

• leukocytes show intermittent interactions with endothelium causing an increase in rolling velocity to ~129 um/second (~35 um/second in wild-type)

• treatment with Tnfa (tumor necrosis factor alpha) reduces rolling velocity to ~5 um/second

increased leukocyte cell number ( J:31374 )

• systemic leukocyte counts are ~9800/ul (~61% neutrophils, ~37% lymphocytes) compared to wild-type counts of ~5660/ul (53% neutrophils, 46% lymphocytes)

cellular

abnormal leukocyte tethering or rolling ( J:31374 )

• after surgery to exteriorize cremaster muscle, mice do not display leukocyte rolling for the first hour, but a significant amount of rolling is detected after 2 hours (~8% rolling leukocyte flux)

• leukocytes show intermittent interactions with endothelium causing an increase in rolling velocity to ~129 um/second (~35 um/second in wild-type)

• treatment with Tnfa (tumor necrosis factor alpha) reduces rolling velocity to ~5 um/second

Genotype
MGI:3766951

hm5

• Allelic Composition: Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

hematopoietic system

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mutants and this increases with age of mice

immune system

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mutants and this increases with age of mice

Genotype
MGI:3606578

hm6

• Allelic Composition: Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

immune system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 61-69% after 2-4 hours

increased leukocyte cell number ( J:101979 )

• elevated peripheral leukocyte count in contrast to controls following infection with S. pneumoniae

increased neutrophil cell number ( J:101979 , J:24239 )

• mild neutrophilia in contrast to controls following infection with S. pneumoniae (J:101979)

• 2-3 fold increase in numbers of circulating neutrophils (J:24239)

abnormal spleen morphology ( J:101979 )

• increase in splenic thrombosis and necrosis in contrast to controls following infection with S. pneumoniae

eye inflammation ( J:101979 )

• panophthalmitis observed in 8% of mice following infection with S. pneumoniae

increased susceptibility to bacterial infection ( J:101979 )

• severity and duration of morbidity higher than wild-type after infection with Streptococcus pneumoniae

• survival rate was 19% in contrast to a 57% rate for wild-type mice

• decreased ability to clear bacteremia among survivors

behavior/neurological

abnormal pilomotor reflex ( J:101979 )

• observed following infection with S. pneumoniae

tremors ( J:101979 )

• observed following infection with S. pneumoniae

head tilt ( J:101979 )

• observed following infection with S. pneumoniae

decreased locomotor activity ( J:101979 )

• observed following infection with S. pneumoniae

spinning ( J:101979 )

• observed following infection with S. pneumoniae

liver/biliary system

hepatic necrosis ( J:101979 )

• higher incidence in contrast to controls following infection with S. pneumoniae

growth/size/body

weight loss ( J:101979 )

• observed 48 hours post-infection with S. pneumoniae

vision/eye

eye inflammation ( J:101979 )

• panophthalmitis observed in 8% of mice following infection with S. pneumoniae

hematopoietic system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 61-69% after 2-4 hours

increased leukocyte cell number ( J:101979 )

• elevated peripheral leukocyte count in contrast to controls following infection with S. pneumoniae

increased neutrophil cell number ( J:101979 , J:24239 )

• mild neutrophilia in contrast to controls following infection with S. pneumoniae (J:101979)

• 2-3 fold increase in numbers of circulating neutrophils (J:24239)

abnormal spleen morphology ( J:101979 )

• increase in splenic thrombosis and necrosis in contrast to controls following infection with S. pneumoniae

cellular

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis reduced neutrophil emigration into peritoneum by 61-69% after 2-4 hours

Genotype
MGI:3767011

cx7

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: B6.129S7-Icam1^tm1Bay Selp^tm1Bay/J

nervous system

nervous system phenotype ( J:119906 )

N • no significant differences are detected in motor function (assessed at 1-5 days after CCI) or cognitive function (assessed at 14-20 days after injury) between mutants and wild-type mice

N • no significant differences are seen in contusion volume of the injured hemisphere or in volume of uninjured or injured hemisphere between wild-type and mutants 21 days after CCI

immune system

immune system phenotype ( J:119906 )

N • no difference in neutrophil accumulation at injury site at 24 hours after CCI is detected between mutant and wild-type mice

homeostasis/metabolism

edema ( J:119906 )

• brain edema at 24 hours after controlled cortical impact (CCI) is decreased in mutants compared to controls; brain water content ratio of injured and uninjured hemispheres) is lower (1.90) than in controls (3.16)

Genotype
MGI:3766607

cx8

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: either: B6.129S7-Selp^tm1Bay Icam1^tm1Bay or (involves: 129S7/SvEvBrd * C57BL/6)

immune system

impaired leukocyte tethering or rolling ( J:31374 )

• double mutants show no spontaneous rolling leukocyte activity

• treatment with Tnfa induces leukocyte rolling although leukocytes show no spontaneous rolling activity; rolling flux fraction is ~22%, compared to ~36% in Icam1-deficient single mutants

cellular

impaired leukocyte tethering or rolling ( J:31374 )

• double mutants show no spontaneous rolling leukocyte activity

• treatment with Tnfa induces leukocyte rolling although leukocytes show no spontaneous rolling activity; rolling flux fraction is ~22%, compared to ~36% in Icam1-deficient single mutants

hematopoietic system

impaired leukocyte tethering or rolling ( J:31374 )

• double mutants show no spontaneous rolling leukocyte activity

• treatment with Tnfa induces leukocyte rolling although leukocytes show no spontaneous rolling activity; rolling flux fraction is ~22%, compared to ~36% in Icam1-deficient single mutants

Genotype
MGI:3766947

cx9

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Sele^tm2Alb/Sele^tm2Alb; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

immune system

impaired neutrophil chemotaxis ( J:112286 )

• migration is completely defective in acute croton oil dermatitis model in young mice (7-14 weeks); older mice show complete abrogation of neutrophil migration in response to irritation

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mice with acute croton oil dermatitis

decreased acute inflammation ( J:112286 )

• in response to croton oil application to the ear in young mice (7-14 weeks), inflammation is significantly reduced relative to controls

hematopoietic system

impaired neutrophil chemotaxis ( J:112286 )

• migration is completely defective in acute croton oil dermatitis model in young mice (7-14 weeks); older mice show complete abrogation of neutrophil migration in response to irritation

increased neutrophil cell number ( J:112286 )

• circulating neutrophils are increased in mice with acute croton oil dermatitis

homeostasis/metabolism

skin edema ( J:112286 )

• dermal edema is decreased by 41% within 6 hours of croton oil irritation in young mice (7-14 weeks), and partial suppression of edema in older (23-35 weeks) mice

integument

integument phenotype ( J:112286 )

N • triply deficient mice do not develop spontaneous skin lesions up to 55 weeks of age

skin edema ( J:112286 )

• dermal edema is decreased by 41% within 6 hours of croton oil irritation in young mice (7-14 weeks), and partial suppression of edema in older (23-35 weeks) mice

cellular

impaired neutrophil chemotaxis ( J:112286 )

• migration is completely defective in acute croton oil dermatitis model in young mice (7-14 weeks); older mice show complete abrogation of neutrophil migration in response to irritation

Genotype
MGI:3766950

cx10

• Allelic Composition: Sele^tm2Alb/Sele^tm2Alb; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

immune system

impaired leukocyte tethering or rolling ( J:70682 )

• rolling is severely compromised

• rolling flux and rolling fraction are reduced relative to wild-type

increased leukocyte cell number ( J:70682 )

• white blood cell counts (total, eosinophil, neutrophil, monocyte counts) are significantly elevated compared to wild-type

increased eosinophil cell number ( J:70682 )

increased neutrophil cell number ( J:70682 , J:112286 )

• circulating neutrophils are increased in mutants and this increases with age of mice (J:112286)

• circulating neutrophils are increased to a greater extent in older mutants showing spontaneous lesions than in those without spontaneous lesions (J:112286)

increased monocyte cell number ( J:70682 )

abnormal spleen B cell follicle morphology ( J:70682 )

• lymphoid follicles forming the white pulp are effaced and infrequently observed due to expansion of the red pulp by extramedullary hematopoiesis

decreased spleen B cell follicle number ( J:70682 )

abnormal neutrophil physiology ( J:112286 )

• migration is defective in young mice (7-14 weeks) in acute croton oil dermatitis model

• in older mutants (23-35 weeks), neutrophil emigration during irritant dermatitis shows no compromise compared to wild-type

• in young mice (8 weeks) with croton oil-induced lesions on their backs 15 days before acute croton oil-induced dermatitis on the ear, a 5-fold greater emigration of neutrophils to the ear irritation is observed compared to mutants without experimental lesions on their backs, while circulating neutrophil numbers are similar for both groups

abnormal lymph node secondary follicle morphology ( J:70682 )

• structures aren't recognized in mutant cervical lymph nodes

abnormal lymph node germinal center morphology ( J:70682 )

• structures aren't recognized in mutant cervical lymph nodes

enlarged lymph nodes ( J:70682 )

• both old and young mice show severe cervical lymphadenopathy, compared to wild-type or Sell-null mice; condition is more severe than in Sele/Selp/Sell-triple null mice

abnormal cytokine secretion ( J:70682 )

• GM-CSF levels are elevated 6-7-fold above levels in wild-type or Sell-null mice

decreased acute inflammation ( J:112286 )

• standardized volume fraction of emigrated neutrophils in dermis of irritated ears is 0.017 +/- 0.006, compared to 0.317 in irritated ears of wild-type mice

hematopoietic system

impaired leukocyte tethering or rolling ( J:70682 )

• rolling is severely compromised

• rolling flux and rolling fraction are reduced relative to wild-type

extramedullary hematopoiesis ( J:70682 )

• mice show massive extramedullary hematopoiesis with identifiable myeloid and megakaryocytic lineages, and lesser erythroid component

increased leukocyte cell number ( J:70682 )

• white blood cell counts (total, eosinophil, neutrophil, monocyte counts) are significantly elevated compared to wild-type

increased eosinophil cell number ( J:70682 )

increased neutrophil cell number ( J:70682 , J:112286 )

• circulating neutrophils are increased in mutants and this increases with age of mice (J:112286)

• circulating neutrophils are increased to a greater extent in older mutants showing spontaneous lesions than in those without spontaneous lesions (J:112286)

increased monocyte cell number ( J:70682 )

abnormal spleen B cell follicle morphology ( J:70682 )

• lymphoid follicles forming the white pulp are effaced and infrequently observed due to expansion of the red pulp by extramedullary hematopoiesis

decreased spleen B cell follicle number ( J:70682 )

abnormal neutrophil physiology ( J:112286 )

• migration is defective in young mice (7-14 weeks) in acute croton oil dermatitis model

• in older mutants (23-35 weeks), neutrophil emigration during irritant dermatitis shows no compromise compared to wild-type

• in young mice (8 weeks) with croton oil-induced lesions on their backs 15 days before acute croton oil-induced dermatitis on the ear, a 5-fold greater emigration of neutrophils to the ear irritation is observed compared to mutants without experimental lesions on their backs, while circulating neutrophil numbers are similar for both groups

cardiovascular system

abnormal lung vasculature morphology ( J:70682 )

• in mutants, alveolocapillary walls are engorged with leukocytes; these leukocytes are confined to small vascular spaces and do not infiltrate the interstitial supporting tissue or alveolar and airway spaces

respiratory system

abnormal lung morphology ( J:70682 )

• lung tissue displays decreasing cellularity within alveolocapillary walls with severely affected interstitial areas

abnormal lung vasculature morphology ( J:70682 )

• in mutants, alveolocapillary walls are engorged with leukocytes; these leukocytes are confined to small vascular spaces and do not infiltrate the interstitial supporting tissue or alveolar and airway spaces

integument

spontaneous skin ulceration ( J:70682 , J:112286 )

• mice develop mucocutaneous infections or ulcerative dermatitis (J:70682)

• at 15 months, mice show large areas of ulceration on the neck (J:70682)

• mice develop spontaneous skin lesions characterized by polymorphonuclear leukocytes (J:112286)

cellular

impaired leukocyte tethering or rolling ( J:70682 )

• rolling is severely compromised

• rolling flux and rolling fraction are reduced relative to wild-type

Genotype
MGI:2656301

cx11

• Allelic Composition: Sele^tm2Alb/Sele^tm2Alb; Sell^tm2Alb/Sell^tm2Alb; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

immune system

immune system phenotype ( J:70682 )

N • GM-CSF levels are comparable to levels in wild-type or Sell-null mutants; elevation observed in Sele/Selp double null mice is absent

abnormal cellular extravasation ( J:70682 )

• neutrophil influx to the peritoneal cavity during thioglycolate-induced peritonitis is significantly reduced compared to wild-type animals in this model

impaired leukocyte tethering or rolling ( J:70682 )

• rolling is severely compromised; no rolling is seen up to 5 hours after cremaster muscle exteriorization

• rolling flux and rolling fraction are more reduced than the decrease observed in Sele/Selp double null mice

increased leukocyte cell number ( J:70682 )

• white blood cell counts (total, eosinophil, neutrophil, monocyte counts) are significantly elevated compared to wild-type, but are ~half the value found in Sele/Selp double mutants

increased eosinophil cell number ( J:70682 )

increased neutrophil cell number ( J:70682 , J:106550 )

• in liver parenchyma and sinusoids, neutrophil numbers are ~2-fold higher in mutants after Gal/ET treatment; numbers of neutrophils in liver tissue are significantly elevated 4 hours prior to Gal/ET treatment, compared to controls (J:106550)

• more neutrophils accumulate in the hepatic vascular beds (sinusoids and venules) after Gal/ET treatment in mutants than in wild-type controls (J:106550)

increased monocyte cell number ( J:70682 )

abnormal spleen morphology ( J:70682 )

• moderate disruption of splenic architecture is observed

abnormal spleen B cell follicle morphology ( J:70682 )

• lymphoid follicles of the white pulp are identified occasionally and have irregular shapes and sizes

decreased spleen B cell follicle number ( J:106550 )

abnormal spleen B cell follicle shape ( J:106550 )

• irregular

enlarged lymph nodes ( J:70682 )

• both old and young mice show severe cervical lymphadenopathy, compared to wild-type or Sell-null mice; condition is more severe than in Sele/Selp/Sell-triple null mice

abnormal cervical lymph node morphology ( J:70682 )

• both old and young mice show marked cervical lymphadenopathy, compared to wild-type or Sell-null mice; condition is less severe than in Sele/Sell-double null mice

lung inflammation ( J:70682 )

• both old and younger mice show bronchial lymphoid aggregates

hematopoietic system

abnormal cellular extravasation ( J:70682 )

• neutrophil influx to the peritoneal cavity during thioglycolate-induced peritonitis is significantly reduced compared to wild-type animals in this model

impaired leukocyte tethering or rolling ( J:70682 )

• rolling is severely compromised; no rolling is seen up to 5 hours after cremaster muscle exteriorization

• rolling flux and rolling fraction are more reduced than the decrease observed in Sele/Selp double null mice

extramedullary hematopoiesis ( J:70682 )

• mice show moderate extramedullary hematopoiesis in sinusoid of red pulp

increased leukocyte cell number ( J:70682 )

• white blood cell counts (total, eosinophil, neutrophil, monocyte counts) are significantly elevated compared to wild-type, but are ~half the value found in Sele/Selp double mutants

increased eosinophil cell number ( J:70682 )

increased neutrophil cell number ( J:70682 , J:106550 )

• in liver parenchyma and sinusoids, neutrophil numbers are ~2-fold higher in mutants after Gal/ET treatment; numbers of neutrophils in liver tissue are significantly elevated 4 hours prior to Gal/ET treatment, compared to controls (J:106550)

• more neutrophils accumulate in the hepatic vascular beds (sinusoids and venules) after Gal/ET treatment in mutants than in wild-type controls (J:106550)

increased monocyte cell number ( J:70682 )

abnormal spleen morphology ( J:70682 )

• moderate disruption of splenic architecture is observed

abnormal spleen B cell follicle morphology ( J:70682 )

• lymphoid follicles of the white pulp are identified occasionally and have irregular shapes and sizes

decreased spleen B cell follicle number ( J:106550 )

abnormal spleen B cell follicle shape ( J:106550 )

• irregular

respiratory system

lung inflammation ( J:70682 )

• both old and younger mice show bronchial lymphoid aggregates

abnormal lung morphology ( J:70682 )

• lung tissue displays decreasing cellularity within alveolocapillary walls, but this is less severe than in Sele/Selp double-nulls

abnormal lung vasculature morphology ( J:70682 )

• only a small increase in leukocytes in alveolocapillary walls are observed and occasional small bronchial lymphoid aggregates are found

cardiovascular system

abnormal lung vasculature morphology ( J:70682 )

• only a small increase in leukocytes in alveolocapillary walls are observed and occasional small bronchial lymphoid aggregates are found

liver/biliary system

hepatic necrosis ( J:106550 )

• at 7 hours after galactosamine/bacterial endotoxin (Gal/ET) treatment, area on necrosis is attenuated 68% compared to treated controls

abnormal liver physiology ( J:106550 )

• mutants show decreased liver injury relative to treated controls at 7 hours after treatment with Gal/ET

homeostasis/metabolism

decreased circulating alanine transaminase level ( J:106550 )

• at 7 hours after galactosamine/bacterial endotoxin (Gal/ET) treatment, plasma ALT levels are reduced by 65% compared to treated controls

integument

integument phenotype ( J:70682 )

N • mice do not show skin ulcerations as seen in double Sele/Selp mutants

cellular

abnormal cellular extravasation ( J:70682 )

• neutrophil influx to the peritoneal cavity during thioglycolate-induced peritonitis is significantly reduced compared to wild-type animals in this model

impaired leukocyte tethering or rolling ( J:70682 )

• rolling is severely compromised; no rolling is seen up to 5 hours after cremaster muscle exteriorization

• rolling flux and rolling fraction are more reduced than the decrease observed in Sele/Selp double null mice

Genotype
MGI:3606634

cx12

• Allelic Composition: Sele^tm2Alb/Sele^tm2Alb; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

immune system

abnormal leukocyte cell number ( J:101979 )

• elevated peripheral leukocyte count (3 fold) relative to controls prior to and following infection

• decreased peritoneal WBC count relative to peripheral WBC count following infection

increased neutrophil cell number ( J:101979 )

• neutrophilia in contrast to controls following infection with S. pneumoniae

• decreased number of neutrophils in peritoneal fluid relative to peripheral absolute neutrophil counts following infection

eye inflammation ( J:101979 )

• panophthalmitis observed in 8% of mice following infection with S. pneumoniae

increased susceptibility to bacterial infection ( J:101979 )

• severity and duration of morbidity higher than wild-type after infection with Streptococcus pneumoniae

• decreased survival rate after post-infection day 5

• decreased ability to clear bacteremia among survivors

behavior/neurological

abnormal pilomotor reflex ( J:101979 )

• observed following infection with S. pneumoniae

tremors ( J:101979 )

• observed following infection with S. pneumoniae

head tilt ( J:101979 )

• observed following infection with S. pneumoniae

decreased locomotor activity ( J:101979 )

• observed following infection with S. pneumoniae

spinning ( J:101979 )

• observed following infection with S. pneumoniae

growth/size/body

weight loss ( J:101979 )

• 48 hours post-infection with S. pneumoniae

vision/eye

eye inflammation ( J:101979 )

• panophthalmitis observed in 8% of mice following infection with S. pneumoniae

hematopoietic system

abnormal leukocyte cell number ( J:101979 )

• elevated peripheral leukocyte count (3 fold) relative to controls prior to and following infection

• decreased peritoneal WBC count relative to peripheral WBC count following infection

increased neutrophil cell number ( J:101979 )

• neutrophilia in contrast to controls following infection with S. pneumoniae

• decreased number of neutrophils in peritoneal fluid relative to peripheral absolute neutrophil counts following infection

Genotype
MGI:3606608

cx13

• Allelic Composition: Icam1^tm1Bay/Icam1^tm1Bay; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

immune system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis eliminated neutrophil emigration into peritoneum

• Streptococcus pneumoniae induced pneumonia did not reduce neutrophil recruitment or edema formation in the alveolar space

increased neutrophil cell number ( J:24239 )

• 4-5 fold increase in numbers of circulating neutrophils

hematopoietic system

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis eliminated neutrophil emigration into peritoneum

• Streptococcus pneumoniae induced pneumonia did not reduce neutrophil recruitment or edema formation in the alveolar space

increased neutrophil cell number ( J:24239 )

• 4-5 fold increase in numbers of circulating neutrophils

cellular

abnormal leukocyte migration ( J:24239 )

• Streptococcus pneumoniae induced peritonitis eliminated neutrophil emigration into peritoneum

• Streptococcus pneumoniae induced pneumonia did not reduce neutrophil recruitment or edema formation in the alveolar space

Genotype
MGI:3799723

cx14

• Allelic Composition: Fas^lpr/Fas^lpr; Selp^tm1Bay/Selp^tm1Bay
• Genetic Background: MRL.Cg-Selp^tm1Bay Fas^lpr

mortality/aging

premature death ( J:127199 )

• overall survival is reduced compared to Fas^lpr homozygotes (median survival is 20 weeks vs 26 weeks for Fas mutants); renal lesions are severe at time of death

immune system

abnormal leukocyte adhesion ( J:126009 )

• rolling is dramatically reduced, but not eliminated, in mutants compared to controls

• in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated

impaired leukocyte tethering or rolling ( J:126009 )

• rolling is dramatically reduced, but not eliminated, in mutants compared to controls

• in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated

increased neutrophil cell number ( J:127199 )

• severe neutrophil accumulation at 20 weeks is observed in kidneys

abnormal chemokine secretion ( J:127199 )

• in kidney and cultured primary renal endothelial cells, levels of CCL2 are elevated compared to Fas^lpr controls at 20 weeks; expression levels are increased further upon LPS treatment of cells

glomerulonephritis ( J:127199 )

• at 20 weeks of age, kidneys display higher lesion scores than controls

dermatitis ( J:127199 )

• double mutants show more rapid onset of cutaneous inflammation than Fas^lpr homozygotes

hematopoietic system

abnormal leukocyte adhesion ( J:126009 )

• rolling is dramatically reduced, but not eliminated, in mutants compared to controls

• in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated

impaired leukocyte tethering or rolling ( J:126009 )

• rolling is dramatically reduced, but not eliminated, in mutants compared to controls

• in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated

increased neutrophil cell number ( J:127199 )

• severe neutrophil accumulation at 20 weeks is observed in kidneys

renal/urinary system

abnormal renal glomerular capsule morphology ( J:127199 )

• at 20 weeks of age, severely affected glomeruli display capsular fibrosis and proliferation of the lining of Bowman's capsule

fused podocyte foot processes ( J:127199 )

• at 20 weeks of age, foot processes are fused

podocyte foot process effacement ( J:127199 )

• at 20 weeks of age, foot processes are diffusely effaced

abnormal renal glomerulus morphology ( J:127199 )

• lesions at 20 weeks are characterized by neutrophil infiltration of the glomerular tuft, proliferation of mesangial and endothelial cells, mild multifocal tubular atrophy, and interstitial mixed inflammatory cell accumulation

• more severely affected glomeruli have necrosis of large areas of the tuft, fibrin deposition, proliferation of lining of Bowman's capsule with fusion of the tuft (synechia), capsular fibrosis, and pericapsular lymphocyte accumulation

• subepithelial and subendothelial electron-dense deposits are detected

abnormal glomerular capillary endothelium morphology ( J:127199 )

• at 20 weeks of age, proliferation of endothelial cells is observed

increased mesangial cell number ( J:127199 )

• at 20 weeks of age, cellularity of mesangium is moderately increased

glomerulonephritis ( J:127199 )

• at 20 weeks of age, kidneys display higher lesion scores than controls

expanded mesangial matrix ( J:127199 )

• at 20 weeks of age, markedly expanded mesangium due to mesangial matrix increase is observed

glomerular crescent ( J:127199 )

• at 20 weeks of age, proliferation of lining of Bowman's capsule is observed

renal glomerular synechia ( J:127199 )

• at 20 weeks of age, proliferation of lining of Bowman's capsule with fusion of the tuft (synechia) is observed

renal glomerulus fibrosis ( J:127199 )

• at 20 weeks of age, severely affected glomeruli exhibit fibrin deposition

renal tubule atrophy ( J:127199 )

• at 20 weeks of age, mild multifocal tubular atrophy is observed

renal necrosis ( J:127199 )

• at 20 weeks of age, severely affected glomeruli display necrosis of large areas of the tuft

kidney failure ( J:127199 )

• progressive decline in renal function is observed, during progression to end-stage renal disease

cardiovascular system

abnormal glomerular capillary endothelium morphology ( J:127199 )

• at 20 weeks of age, proliferation of endothelial cells is observed

vascular inflammation ( J:127199 )

integument

dermatitis ( J:127199 )

• double mutants show more rapid onset of cutaneous inflammation than Fas^lpr homozygotes

cellular

increased mesangial cell number ( J:127199 )

• at 20 weeks of age, cellularity of mesangium is moderately increased

abnormal leukocyte adhesion ( J:126009 )

• rolling is dramatically reduced, but not eliminated, in mutants compared to controls

• in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated

impaired leukocyte tethering or rolling ( J:126009 )

• rolling is dramatically reduced, but not eliminated, in mutants compared to controls

• in mice chronically treated with anti-E-selectin antibodies, rolling is completely eliminated