Induction of specific clonal anergy in human T lymphocytes by Staphylococcus aureus enterotoxins.
Induction of specific clonal anergy in human T lymphocytes by Staphylococcus aureus enterotoxins.
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金黄色葡萄球菌肠毒素诱导人 T 淋巴细胞特异性克隆无反应性。
DOI：
10.1073/pnas.87.22.8884
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发表时间：
1990
影响因子：
11.1
通讯作者：
Jonathan R. Lamb
中科院分区：
文献类型：
--
作者：
Robyn E O'Hehir;Jonathan R. Lamb
由某些金黄色葡萄球菌菌株产生的外毒素能够刺激强大的多克隆增殖反应，并通过克隆缺失表达适当T细胞抗原受体V β基因产物的T淋巴细胞诱导无反应性。本文考察了S.金黄色葡萄球菌肠毒素以调节具有确定的抗原特异性的人CD 4 + T淋巴细胞的反应性。观察到某些S.金黄色葡萄球菌毒素能够激活和诱导表达V β 3+元件的血凝素反应性T细胞的无反应性。经S.金黄色葡萄球菌肠毒素A、B和D，尽管对外源性白细胞介素2的增殖增强，但T细胞不能应答以免疫原性形式呈递的其天然配体。色葡萄金黄色葡萄球菌毒素诱导的无反应性与T细胞膜受体的调节有关; T细胞抗原受体的下调伴随着CD 2和CD 25表达的增强。有趣的是，CD 28仅在刺激时增加，表明这种蛋白质可能由活化和无反应性T细胞差异表达。这些结果表明，细菌毒素能够诱导抗原特异性无反应性的人T细胞，其应用可能是相关的T细胞表达的V β基因产物的一个特定的家庭的调节。
The exotoxins produced by certain strains of Staphylococcus aureus are able to stimulate powerful polyclonal proliferative responses and to induce nonresponsiveness by clonal deletion of T lymphocytes expressing the appropriate T-cell antigen receptor V beta gene products. This paper examines the ability of S. aureus enterotoxins to modulate the responsiveness of human CD4+ T lymphocytes with defined antigen specificity. It was observed that certain S. aureus toxins were able to activate and induce anergy in hemagglutinin-reactive T cells expressing V beta 3+ elements. After exposure to S. aureus enterotoxins A, B, and D in the absence of antigen-presenting cells, the T cells failed to respond to their natural ligand presented in an immunogenic form, despite enhanced proliferation to exogenous interleukin 2. The S. aureus toxin-induced anergy was associated with modulation of T-cell membrane receptors; down-regulation of the T-cell antigen receptor was concomitant with enhanced expression of CD2 and CD25. Interestingly, CD28 was increased only on stimulation, suggesting this protein may be differentially expressed by activated and anergic T cells. These results indicate that bacterial toxins are able to induce antigen-specific nonresponsiveness in human T cells, the application of which may be relevant in the regulation of T cells expressing a particular family of V beta gene products.