Udaka K, Marusić-Galesić S, Walden P
Max Planck Institute for Biology, Department of Immunogenetics, Tübingen, Germany.
J Immunol. 1994 Sep 15;153(6):2843-50.
Despite original reports that describe the absence of CD8+ CTLs in mice having homozygous deficiency in the beta 2-microglobulin gene, strong cytotoxic activities against cells with normal beta 2-microglobulin expression were observed in these animals. This cytotoxicity was reproducibly induced by immunizations with allogeneic or syngeneic cells. MHC class II expression by the stimulator cells was not required. The effector population contained alpha beta T cells with CD4+ or CD8+ phenotypes, as well as gamma delta T cells with CD8- and CD8+ phenotypes. Both alpha beta T cell types recognized MHC class I molecules. The gamma delta T cells seemed to respond to molecules that are affected by the absence of beta 2-microglobulin, but that are not encoded by classical MHC loci.
尽管最初的报告描述了β2-微球蛋白基因纯合缺陷的小鼠中不存在CD8+细胞毒性T淋巴细胞(CTL),但在这些动物中观察到了针对具有正常β2-微球蛋白表达的细胞的强大细胞毒性活性。这种细胞毒性可通过用同种异体或同基因细胞免疫而反复诱导。刺激细胞的MHC II类表达不是必需的。效应细胞群体包含具有CD4+或CD8+表型的αβT细胞,以及具有CD8-和CD8+表型的γδT细胞。两种αβT细胞类型都识别MHC I类分子。γδT细胞似乎对受β2-微球蛋白缺失影响但不由经典MHC基因座编码的分子作出反应。