Choi Y, Lafferty J A, Clements J R, Todd J K, Gelfand E W, Kappler J, Marrack P, Kotzin B L
Howard Hughes Medical Institute, Denver.
J Exp Med. 1990 Sep 1;172(3):981-4. doi: 10.1084/jem.172.3.981.
Infection with Staphylococcus aureus and the production of toxic shock syndrome toxin-1 (TSST-1) have been implicated in the pathogenesis of toxic shock syndrome. Previous in vitro studies have demonstrated that TSST-1 is a powerful but selective stimulator of human T cells, and that the majority of activated cells express the TCR V beta 2 gene segment. We therefore studied patients with toxic shock syndrome using a modification of the PCR to determine if expansion of V beta 2+ T cells is a marker of the in vivo disease process. Five of eight patients studied demonstrated markedly elevated levels of circulating V beta 2+ T cells, whereas none showed significantly elevated levels of T cells expressing other V beta gene segments. The results suggest that toxin-mediated T cell activation, which involves a large fraction of the human T cell repertoire, may be critical in the pathogenesis of this disease.
金黄色葡萄球菌感染及毒性休克综合征毒素-1(TSST-1)的产生与毒性休克综合征的发病机制有关。先前的体外研究表明,TSST-1是人类T细胞的一种强大但具有选择性的刺激物,并且大多数活化细胞表达TCR Vβ2基因片段。因此,我们使用改良的聚合酶链反应(PCR)研究了毒性休克综合征患者,以确定Vβ2 + T细胞的扩增是否是体内疾病过程的一个标志物。在研究的8名患者中,有5名患者循环Vβ2 + T细胞水平明显升高,而没有患者显示表达其他Vβ基因片段的T细胞水平显著升高。结果表明,涉及大部分人类T细胞库的毒素介导的T细胞活化可能在该疾病的发病机制中起关键作用。