Phenotypes Associated with This Genotype

Genotype
MGI:3029024

• Allelic Composition: Ticam1^tm1Aki/Ticam1^tm1Aki
• Genetic Background: involves: 129P2/OlaHsd

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

immune system

decreased splenocyte proliferation ( J:84679 )

• splenocytes show defective proliferation in response to poly(I:C) or LPS

abnormal B cell physiology ( J:84679 )

• B-cells are impaired in poly(I:C) augmentation of surface expression of CD69, CD86, and MHC class

abnormal B cell activation ( J:174941 )

• enhanced rEA stimulated activation of B cells compared to wild-type controls

abnormal NK cell physiology ( J:174941 )

• enhanced rEA stimulated activation of NK cells compared to wild-type controls

abnormal NK T cell physiology ( J:174941 )

• enhanced rEA stimulated activation of NK T cells compared to wild-type controls

abnormal macrophage physiology ( J:84679 , J:174941 )

• LPS-induced production of tumor necrosis factor-alpha and IL-12 p40 is abolished in mutant macrophages (J:84679)

• enhanced rEA stimulated activation of macrophages compared to wild-type controls (J:174941)

impaired macrophage phagocytosis ( J:185198 )

• in culture the clearance of axonal debris by peritoneal macrophages from degenerating axons is markedly reduced

• in vivo axonal phagocytosis by microglia is reduced following axon degeneration induced by lumbar dorsal root axotomy

abnormal microglial cell physiology ( J:185198 )

• in culture the clearance of axonal debris from degenerating axons and following axotomy is reduced

• in culture following axotomy microglia exhibit slightly slower migration toward axonal debris and a decreased capacity to engulf material

• in vivo axonal phagocytosis is reduced following axon degeneration induced by lumbar dorsal root axotomy

abnormal cytokine level ( J:174941 )

• enhanced rEA stimulated increase in cytokine and chemokine levels

abnormal interleukin level ( J:137522 )

• severely impaired production of IL12p40

decreased circulating interleukin-6 level ( J:145306 )

• following exposure to acid-induced acute lung injury, LPS, or 1-palmitoyl-2-arachidonoyl-phosphatidylcholine

abnormal dendritic cell physiology ( J:174941 )

• enhanced Eimeria tenella derived antigen (rEA) stimulated activation of dendritic cells compared to wild-type controls

• dendritic cells produce dramatically higher levels of cytokines when stimulated with LPS, R848 or ODN2006 compared to wild-type cells

abnormal cytokine secretion ( J:84679 )

• mutants show defective production of inflammatory cytokines in response to LPS

• LPS-induced production of tumor necrosis factor-alpha and IL-12 p40 is abolished in mutant macrophages

decreased susceptibility to endotoxin shock ( J:84679 )

• mutants show defective production of inflammatory cytokines and resistance to LPS-induced septic shock

decreased susceptibility to Orthomyxoviridae infection ( J:145306 )

• following exposure to inactivated H5N1 virus , acute-lung injury and IL6 production are attenuated compared to in wild-type mice

homeostasis/metabolism

abnormal cytokine level ( J:174941 )

• enhanced rEA stimulated increase in cytokine and chemokine levels

abnormal interleukin level ( J:137522 )

• severely impaired production of IL12p40

decreased circulating interleukin-6 level ( J:145306 )

• following exposure to acid-induced acute lung injury, LPS, or 1-palmitoyl-2-arachidonoyl-phosphatidylcholine

decreased susceptibility to injury ( J:145306 )

• following exposure to acid-induced acute lung injury, mice exhibit alleviated symptoms compared to wild-type mice with decreased changes in elastance, edema, and serum IL6 levels

• following exposure to 1-palmitoyl-2-arachidonoyl-phosphatidylcholine, lung function is improved and IL6 production is decreased compared to in similarly treated wild-type mice

hematopoietic system

decreased splenocyte proliferation ( J:84679 )

• splenocytes show defective proliferation in response to poly(I:C) or LPS

abnormal B cell physiology ( J:84679 )

• B-cells are impaired in poly(I:C) augmentation of surface expression of CD69, CD86, and MHC class

abnormal B cell activation ( J:174941 )

• enhanced rEA stimulated activation of B cells compared to wild-type controls

abnormal NK cell physiology ( J:174941 )

• enhanced rEA stimulated activation of NK cells compared to wild-type controls

abnormal NK T cell physiology ( J:174941 )

• enhanced rEA stimulated activation of NK T cells compared to wild-type controls

abnormal macrophage physiology ( J:84679 , J:174941 )

• LPS-induced production of tumor necrosis factor-alpha and IL-12 p40 is abolished in mutant macrophages (J:84679)

• enhanced rEA stimulated activation of macrophages compared to wild-type controls (J:174941)

impaired macrophage phagocytosis ( J:185198 )

• in culture the clearance of axonal debris by peritoneal macrophages from degenerating axons is markedly reduced

• in vivo axonal phagocytosis by microglia is reduced following axon degeneration induced by lumbar dorsal root axotomy

abnormal microglial cell physiology ( J:185198 )

• in culture the clearance of axonal debris from degenerating axons and following axotomy is reduced

• in culture following axotomy microglia exhibit slightly slower migration toward axonal debris and a decreased capacity to engulf material

• in vivo axonal phagocytosis is reduced following axon degeneration induced by lumbar dorsal root axotomy

cellular

decreased splenocyte proliferation ( J:84679 )

• splenocytes show defective proliferation in response to poly(I:C) or LPS

impaired macrophage phagocytosis ( J:185198 )

• in culture the clearance of axonal debris by peritoneal macrophages from degenerating axons is markedly reduced

• in vivo axonal phagocytosis by microglia is reduced following axon degeneration induced by lumbar dorsal root axotomy

nervous system

abnormal microglial cell physiology ( J:185198 )

• in culture the clearance of axonal debris from degenerating axons and following axotomy is reduced

• in culture following axotomy microglia exhibit slightly slower migration toward axonal debris and a decreased capacity to engulf material

• in vivo axonal phagocytosis is reduced following axon degeneration induced by lumbar dorsal root axotomy