Poindexter N J, Schlievert P M
J Infect Dis. 1987 Jul;156(1):122-9. doi: 10.1093/infdis/156.1.122.
Toxic-shock-syndrome toxin-1 (TSST-1), produced by Staphylococcus aureus and associated with toxic shock syndrome, functions in vitro as both a lymphoproliferative and immunosuppressive protein for human peripheral blood mononuclear cells (PBMs). We analyzed TSST-1-target cell interactions by receptor-ligand binding analyses. In competitive binding experiments, 2 X 10(5) human PBMs or purified cell populations were incubated in the presence of small amounts of (5-50 ng) of 125I-labeled TSST-1 and increasing amounts of unlabeled TSST-1 (25-10,000 ng). Data were analyzed by the method of Scatchard. Toxin-specific receptors were shown to exist on T lymphocytes within the PBM population. T4+ cells had 27.5 X 10(6) receptors per cell, and T8+ cells had 9 X 10(6) receptors per cell. T4+ and T8+ receptors had dissociation constants of 2.58 X 10(-8) M and 1.8 X 10(-8) M, respectively. These studies confirm earlier work showing that TSST-1 causes the functional activation of a population of T lymphocytes involved in suppression of immunoglobulin responses.
中毒性休克综合征毒素-1（TSST-1）由金黄色葡萄球菌产生，与中毒性休克综合征相关，在体外对人外周血单个核细胞（PBMs）具有淋巴细胞增殖和免疫抑制蛋白的功能。我们通过受体-配体结合分析来分析TSST-1与靶细胞的相互作用。在竞争性结合实验中，将2×10⁵个人类PBMs或纯化的细胞群体与少量（5 - 50 ng）的¹²⁵I标记的TSST-1以及递增剂量的未标记TSST-1（25 - 10000 ng）一起孵育。数据采用Scatchard方法进行分析。结果表明，毒素特异性受体存在于PBM群体中的T淋巴细胞上。T4⁺细胞每个细胞有27.5×10⁶个受体，T8⁺细胞每个细胞有9×10⁶个受体。T4⁺和T8⁺受体的解离常数分别为2.58×10⁻⁸ M和1.8×10⁻⁸ M。这些研究证实了早期的工作，即TSST-1可导致参与抑制免疫球蛋白反应的一群T淋巴细胞的功能激活。
