mortality/aging
• there is a 35% mortality rate resulting from colitis compared to 8.3% mortality of Tcratm1Mom homozygote controls
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digestive/alimentary system
• mice have a higher incidence of colitis and a more severe disease than control mice that are only homozygote for the Tcratm1Mom null allele
• 83% of mice have colitis compared to 14% of controls at 30 weeks of age
• the first signs of disease occur at 15 weeks of age compared to 20 weeks of age in controls
• higher incidence of pathological lesions occurs in the colon of these mice, including loss of goblet cells, elongation of crypts, and inflammatory infiltration of the colon walls
• there is a 35% mortality rate resulting from colitis compared to 8.3% of controls
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immune system
• mice have a higher incidence of colitis and a more severe disease than control mice that are only homozygote for the Tcratm1Mom null allele
• 83% of mice have colitis compared to 14% of controls at 30 weeks of age
• the first signs of disease occur at 15 weeks of age compared to 20 weeks of age in controls
• higher incidence of pathological lesions occurs in the colon of these mice, including loss of goblet cells, elongation of crypts, and inflammatory infiltration of the colon walls
• there is a 35% mortality rate resulting from colitis compared to 8.3% of controls
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• mice have higher numbers of gamma-delta and TCRbeta-beta IEL in the colon both before and after the onset of colitis compared to Tcratm1Mom homozygote controls
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• mesenteric lymph nodes are enlarged in these mice with about a 2-fold increase in cell number compared to Tcratm1Mom homozygote controls
• this increase in cellularity occurs regardless if mice have developed colitis or not
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• TCRbeta-beta T cells isolated from the mesenteric lymph nodes produce around 4-fold more IL-4 than controls
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hematopoietic system
• mice have higher numbers of gamma-delta and TCRbeta-beta IEL in the colon both before and after the onset of colitis compared to Tcratm1Mom homozygote controls
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