Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

摘要: Abstract The T cell antigen receptor (TCR)-associated invariable membrane proteins (CD3-gamma, -delta, -epsilon and -zeta) are critical to the assembly surface expression of TCR/CD3 complex signal transduction upon engagement TCR with antigen. Disruption CD3-zeta gene by homologous recombination resulted in a structurally abnormal thymus which primarily contained CD4- CD8- TCR/CD3very lowCD4+CD8+ cells. Spleen lymph nodes CD3-zeta-/- mutant mice normal number ratio CD4+ CD8+ single positive cells that were low. These splenocytes did not respond antibody cross-linking or mitogenic triggering. The V beta genes CD4-CD8- CD4+CD8+ thymocytes splenic productively rearranged. data demonstrated (i) absence chain, could differentiate low thymocytes, (ii) thymic selection might have occurred, (iii) but transition CD4+CD8- CD4-CD8+ took place at very rate. Most strikingly, intraepithelial lymphocytes (IELs) isolated from small intestine colon expressed levels complexes on their Fc epsilon RI gamma homodimers. In contrast containing IELs, these failed proliferate after triggering mitogen. comparison thymus-derived peripheral spleen nodes, preferential intestinal IELs suggested they mature via an independent extrathymic pathway.