Rao A, Faas S J, Miller L J, Riback P S, Cantor H
J Exp Med. 1983 Oct 1;158(4):1243-58. doi: 10.1084/jem.158.4.1243.
We describe a sequence of reciprocal interactions between cloned inducer T cells and antigen-presenting cells (APC) that results in selective depletion of the antigen-reactive inducer cells. We show that corecognition of antigen and I-A by hapten-reactive inducer T cell clones results in (a) release of macrophage-activating factor (MAF) and other lymphokines, (b) expression of lytic activity by a subset of MAF-sensitized APC after triggering, and (3) lysis (mediated by the activated and triggered macrophage) of the inducer T cell clone and other cells in the vicinity. We suggest that this sequence of steps may limit the extent of macrophage-mediated tissue destruction by depleting the specific inducer T cell clones that initiate the response.
我们描述了克隆诱导性T细胞与抗原呈递细胞(APC)之间一系列相互作用的过程,这些相互作用导致抗原反应性诱导细胞的选择性耗竭。我们发现,半抗原反应性诱导性T细胞克隆对抗原和I-A的共同识别会导致:(a)巨噬细胞激活因子(MAF)和其他淋巴因子的释放;(b)一部分MAF致敏的APC在被触发后表现出溶解活性;以及(3)诱导性T细胞克隆和附近其他细胞被(由活化并被触发的巨噬细胞介导)裂解。我们认为,这一系列步骤可能通过消耗引发反应的特异性诱导性T细胞克隆来限制巨噬细胞介导的组织破坏程度。