葡萄球菌肠毒素B诱导的T细胞无反应性由调节性T细胞介导。
Staphylococcal enterotoxin B-induced T-cell anergy is mediated by regulatory T cells.
作者信息
Wang Z Q, Orlikowsky T, Dudhane A, Trejo V, Dannecker G E, Pernis B, Hoffmann M K
机构信息
Department of Microbiology and Immunology, New York Medical College, Valhalla 10595, USA.
出版信息
Immunology. 1998 Jul;94(3):331-9. doi: 10.1046/j.1365-2567.1998.00519.x.
Naive T cells mount a vigorous proliferative response to superantigen (SAg) stimulation in vivo. The proliferative response is followed by a partial deletion of responder T cells. Part of the deletion process has recently been attributed to the action of regulatory cytotoxic T cells that recognize major histocompatibility complex (MHC) class I-associated antigen receptor determinants on the target cell surface. Responder T cells that survived the SAg response were found to be incapable of generating a secondary proliferative response to a SAg challenge. We show here that this 'anergy' is enforced by CD8-positive regulatory suppressive T cells. These regulatory cells inhibit cell division of preactivated T cells but not the Sag response of naive T cells. Regulatory T cells are not generated in the presence of cyclosporin A and, once activated, become inactivated or deleted when restimulated in the presence of this immunosuppressive drug.
幼稚T细胞在体内对超抗原（SAg）刺激产生强烈的增殖反应。增殖反应之后是反应性T细胞的部分缺失。最近，部分缺失过程被归因于识别靶细胞表面主要组织相容性复合体（MHC）I类相关抗原受体决定簇的调节性细胞毒性T细胞的作用。发现从SAg反应中存活下来的反应性T细胞无法对SAg攻击产生二次增殖反应。我们在此表明，这种“无反应性”是由CD8阳性调节性抑制T细胞强制产生的。这些调节性细胞抑制预激活T细胞的细胞分裂，但不抑制幼稚T细胞的SAg反应。在环孢素A存在的情况下不会产生调节性T细胞，并且一旦被激活，在这种免疫抑制药物存在的情况下再次刺激时会失活或缺失。
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