Hermann E, Lohse A W, Mayet W J, van der Zee R, Van Eden W, Probst P, Poralla T, Meyer zum Büschenfelde K H, Fleischer B
First Department of Medicine, Johannes Gutenberg University, Mainz, Germany.
Clin Exp Immunol. 1992 Sep;89(3):427-33. doi: 10.1111/j.1365-2249.1992.tb06975.x.
T lymphocyte responses to heterologous or self 65-kD heat shock protein (hsp) have been implicated in the pathogenesis of various forms of arthritis. To delineate the relationship of 65-kD hsp to different synovial fluid (SF) T cell subsets, we stimulated synovial fluid (SFMC) and peripheral blood mononuclear cells (PBMC) from patients with different inflammatory rheumatic diseases and from healthy controls with human or mycobacterial 65-kD hsp, tetanus toxoid (TT), heat-killed or live Yersinia enterocolitica. Phenotyping of the resulting T cell lines revealed an increase of up to 97% TCR-gamma delta+ lymphocytes in the 65-kD hsp-stimulated SF-derived lines. This expansion of TCR-gamma delta+ cells was less pronounced with cultures of PBMC. A preferential expansion of TCR-gamma delta+ cells was also shown after SFMC stimulation with live, but not with heat-killed Yersinia or with TT. We conclude that a common mechanism is involved in the selective expansion of TCR-gamma delta+ lymphocytes upon SFMC infection with live Yersinia or upon contact with 65-kD hsp. Out of a panel of TCR-gamma delta+ T lymphocyte clones (TLC) derived from a human 65-kD hsp-stimulated line, only a minority of TLC proliferated weakly upon restimulation with this antigen in the presence of autologous monocytes, whereas TCR-alpha beta+ TLC responded vigorously to the human 65-kD hsp and in some cases also cross-recognized the mycobacterial hsp homologue and/or heat-killed Yersinia. This implies that additional factors or cells may be present in the milieu of SFMC cultures that propagate the expansion of TCR-gamma delta+ cells in response to 65-kD hsp or live bacteria.
T淋巴细胞对异源或自身65-kD热休克蛋白（hsp）的反应与各种形式关节炎的发病机制有关。为了阐明65-kD hsp与不同滑膜液（SF）T细胞亚群的关系，我们用人类或分枝杆菌65-kD hsp、破伤风类毒素（TT）、热灭活或活的小肠结肠炎耶尔森菌刺激来自不同炎性风湿性疾病患者和健康对照者的滑膜液（SFMC）和外周血单核细胞（PBMC）。对所得T细胞系进行表型分析发现，在65-kD hsp刺激的SF来源的细胞系中，TCR-γδ+淋巴细胞增加了高达97%。PBMC培养时，TCR-γδ+细胞的这种扩增不太明显。在用活的小肠结肠炎耶尔森菌刺激SFMC而非热灭活的小肠结肠炎耶尔森菌或TT刺激后，也显示出TCR-γδ+细胞的优先扩增。我们得出结论，在SFMC感染活的小肠结肠炎耶尔森菌或接触65-kD hsp后，TCR-γδ+淋巴细胞的选择性扩增涉及一种共同机制。在一组源自人类65-kD hsp刺激细胞系的TCR-γδ+ T淋巴细胞克隆（TLC）中，只有少数TLC在自体单核细胞存在下再次用该抗原刺激时增殖较弱，而TCR-αβ+ TLC对人类65-kD hsp反应强烈，在某些情况下还交叉识别分枝杆菌hsp同源物和/或热灭活的小肠结肠炎耶尔森菌。这意味着在SFMC培养环境中可能存在其他因素或细胞，它们能促进TCR-γδ+细胞对65-kD hsp或活细菌的扩增反应。
