Ackermann B, Staege M S, Reske-Kunz A B, Dienes H P, Meyer zum Büschenfelde K H, Märker-Hermann E
First Department of Medicine, Johannes Gutenberg-University of Mainz, Germany.
J Infect Dis. 1997 May;175(5):1121-7. doi: 10.1086/516451.
In enterobacteria-induced reactive arthritis (ReA), different T cell subsets play a role in the induction and maintenance of the synovitic process. Synovial fluid-derived alphabeta CD4, alphabeta CD8, and gammadelta T lymphocyte clones (TLC) that recognize Yersinia or Salmonella antigens on professional antigen-presenting cells (APC) have been characterized, and T cells themselves can function as nonprofessional APC. T cells were infected with the facultatively intracellular, arthritogenic enterobacterium Yersinia enterocolitica O:3. A CD8 TLC isolated from a patient with Yersinia-induced ReA recognized and efficiently lysed autologous and allogeneic Yersinia-infected T cells. Infected cytotoxic T lymphocytes (CTL) had a reduced lytic capacity against syngeneic and allogeneic infected target cells, suggesting that the infection of CTL by bacteria may represent a mechanism of immune escape. In ReA, antigen presentation by T cells may modify the antibacterial immune response and may also contribute to network control mechanisms of T cell-mediated cytotoxicity.
在肠杆菌诱导的反应性关节炎(ReA)中,不同的T细胞亚群在滑膜炎过程的诱导和维持中发挥作用。已经对滑膜液来源的αβ CD4、αβ CD8和γδ T淋巴细胞克隆(TLC)进行了表征,这些克隆可识别专职抗原呈递细胞(APC)上的耶尔森菌或沙门氏菌抗原,并且T细胞自身可作为非专职APC发挥作用。用兼性胞内、致关节炎肠杆菌小肠结肠炎耶尔森菌O:3感染T细胞。从一名耶尔森菌诱导的ReA患者中分离出的一个CD8 TLC识别并有效裂解自体和同种异体耶尔森菌感染的T细胞。受感染的细胞毒性T淋巴细胞(CTL)对同基因和同种异体感染靶细胞的裂解能力降低,这表明细菌对CTL的感染可能代表一种免疫逃逸机制。在ReA中,T细胞的抗原呈递可能会改变抗菌免疫反应,也可能有助于T细胞介导的细胞毒性的网络控制机制。