Wack A, Corbella P, Harker N, Crispe I N, Kioussis D
Division of Molecular Immunology, National Institute for Medical Research, London, GB.
Eur J Immunol. 1997 Mar;27(3):577-83. doi: 10.1002/eji.1830270302.
Antigen-triggered activation of T cells leads to a sequence of differentiation steps including up-regulation of activation markers, blast formation, proliferation, delivery of effector functions, and ultimately apoptosis. It is still controversial in which anatomical site activation-induced apoptosis and elimination of T cells occur. To address this question, we used mice transgenic for a T cell receptor (F5) specific for an influenza virus nucleoprotein peptide (NP68) presented on the major histocompatibility complex H-2 Db molecule. Accumulation and apoptosis of T cells was studied using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling in situ combined with immunohistology after intraperitoneal injection of the cognate peptide into F5 mice which are wild type or deficient for Rag-1. After 4 days of peptide treatment, large perivascular infiltrations of CD8+ cells were observed in liver, lung, and kidney of F5 mice. CD8+ cell numbers were also increased in skin and small intestine, but not in brain or heart muscle of peptide-treated animals. The infiltrating CD8+ cells show an increased percentage of apoptosis in liver, lung and, most strikingly, the kidney. These data suggest that in the F5 system, T cell disposal after activation occurs in a number of organs. Essentially identical findings were obtained in Rag-1(+/+) and Rag-1(-/-) F5 mice, suggesting that the deletion mechanism did not involve other T or B cells.
抗原触发的T细胞活化会导致一系列分化步骤,包括活化标志物上调、母细胞形成、增殖、效应功能发挥,最终导致细胞凋亡。T细胞活化诱导的凋亡及清除发生在哪个解剖部位仍存在争议。为解决这个问题,我们使用了针对主要组织相容性复合体H-2 Db分子上呈递的流感病毒核蛋白肽(NP68)的T细胞受体(F5)转基因小鼠。在野生型或Rag-1缺陷的F5小鼠腹腔注射同源肽后,通过末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记原位结合免疫组织学方法,研究T细胞的聚集和凋亡情况。肽处理4天后,在F5小鼠的肝脏、肺和肾脏中观察到大量CD8⁺细胞的血管周围浸润。在肽处理动物的皮肤和小肠中,CD8⁺细胞数量也增加,但在脑或心肌中未增加。浸润的CD8⁺细胞在肝脏、肺中,最显著的是在肾脏中显示出凋亡百分比增加。这些数据表明,在F5系统中,活化后T细胞的清除发生在多个器官中。在Rag-1(+/+)和Rag-1(-/-) F5小鼠中获得了基本相同的结果,表明缺失机制不涉及其他T或B细胞。