Hines W H, Haverty T P, Elias J A, Neilson E G, Kelly C J
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104.
Autoimmunity. 1989;5(1-2):37-47. doi: 10.3109/08916938909029141.
The presentation of self-antigens to circulating T cells is a critical, precipitating event in the induction of autoimmune injury in parenchymal organs. Epithelia expressing these self-antigens are thought to release such moieties for reprocessing by traditional antigen-presenting cells within the lymphoid system. We now demonstrate, however, that some epithelium possess novel functional mechanisms for presenting their own antigens to a responsive, syngeneic T cell repertoire. The presentation of these self-antigens occurs in the context of MHC class II molecules and depends on CD4 associative-recognition determinants. Our findings strongly suggest that organ epithelium may directly activate cell-mediated events to produce autoimmunity through self-recognition.
向循环T细胞呈递自身抗原是实质器官自身免疫损伤诱导过程中的一个关键触发事件。表达这些自身抗原的上皮细胞被认为会释放此类分子，以供淋巴系统内的传统抗原呈递细胞进行再处理。然而，我们现在证明，一些上皮细胞具有将自身抗原呈递给反应性同基因T细胞库的新功能机制。这些自身抗原的呈递发生在MHC II类分子的背景下，并依赖于CD4关联识别决定簇。我们的研究结果强烈表明，器官上皮细胞可能通过自身识别直接激活细胞介导的事件以产生自身免疫。
