Hermann E, Mayet W J, Meyer zum Büschenfelde K H, Fleischer B
First Department of Medicine, Johannes Gutenberg-University of Mainz, Germany.
Cell Immunol. 1992 Sep;143(2):253-60. doi: 10.1016/0008-8749(92)90023-i.
A CD8+ alpha beta TCR+ T cell clone (A35) was isolated from the synovial fluid of a patient with post-enteric reactive arthritis caused by Yersinia enterocolitica. This clone efficiently killed autologous and allogeneic target cells that had been preincubated with live but not with heat-killed bacteria. There was no restriction by polymorphic parts of HLA-A, -B, or -C molecules and a HLA class II-deficient mutant cell line was lysed as efficiently as its normal counterpart, whereas infected HLA class I-deficient cells (Daudi cells) were not. The clone showed crossreaction between Yersinia enterocolitica, Escherichia coli, Pseudomonas aeruginosa, and Streptococcus pyogenes, but did not lyse target cells preincubated with Staphylococcus epidermidis. MAb to CD2, CD3, and CD8 efficiently blocked A35, whereas the addition of mAb to HLA class II or to HLA class I did not. This clone apparently represents a novel effector mechanism against bacteria-infected or -modified cells that could be involved in the immunopathology of reactive arthritis.
从一名由小肠结肠炎耶尔森菌引起的肠后反应性关节炎患者的滑液中分离出一个CD8⁺αβTCR⁺T细胞克隆（A35）。该克隆能有效杀伤预先与活细菌而非热灭活细菌共孵育的自体和异体靶细胞。HLA - A、- B或 - C分子的多态性部分不存在限制，且HLA II类缺陷突变细胞系与其正常对应物一样被高效裂解，而感染的HLA I类缺陷细胞（Daudi细胞）则未被裂解。该克隆在小肠结肠炎耶尔森菌、大肠埃希菌、铜绿假单胞菌和化脓性链球菌之间表现出交叉反应，但不裂解预先与表皮葡萄球菌共孵育的靶细胞。抗CD2、CD3和CD8单克隆抗体能有效阻断A35，而添加抗HLA II类或抗HLA I类单克隆抗体则不能。该克隆显然代表了一种针对细菌感染或修饰细胞的新型效应机制，可能参与反应性关节炎的免疫病理学过程。
