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中毒性休克综合征毒素-1的生物学活性研究:II. 毒素刺激人外周血单个核细胞来源的T细胞诱导增殖反应及白细胞介素2的产生

Study of the biological activities of toxic shock syndrome toxin-1: II. Induction of the proliferative response and the interleukin 2 production by T cells from human peripheral blood mononuclear cells stimulated with the toxin.

作者信息

Uchiyama T, Kamagata Y, Yan X J, Kohno M, Yoshioka M, Fujikawa H, Igarashi H, Okubo M, Awano F, Saito-Taki T

机构信息

Department of Microbiology, Tokyo Women's Medical College, Japan.

出版信息

Clin Exp Immunol. 1987 Jun;68(3):638-47.

PMID:3498581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1542756/
Abstract

Toxic shock syndrome toxin-1 (TSST-1) is an exotoxin produced by Staphylococcus aureus isolated from patients with toxic shock syndrome. We investigated the proliferative response of human lymphocytes and their interleukin 2 (IL-2) production after stimulation with TSST-1 in vitro. Human cord blood mononuclear cells (HCBM) and human peripheral blood mononuclear cells (HPBM) could proliferate with TSST-1 stimulation. T cell-depleted HPBM showed only a marginal response to this toxin. A IL-2-like factor with a molecular weight of 15-18 kD was obtained from the supernatants of TSST-1-stimulated HPBM cultures. The factor was absorbed by CTLL-2 cells but not by T cell-depleted murine spleen cells, indicating that it is IL-2. HPBM are very sensitive to TSST-1: a low concentration of TSST-1 (0.01 ng/ml in 36 h stimulation) and a short period of stimulation (8 h at 10 ng/ml of the toxin) were fully effective for HPBM to produce substantial amounts of IL-2. Removal of T cells abrogated the TSST-1-induced IL-2 production by HPBM. Reconstituted cell cultures of nylon wool column-passed T cells and macrophages produced IL-2 by TSST-1 stimulation and, furthermore, the accessory activity of the macrophages could be partially replaced by a macrophage-derived factor containing interleukin 1. These findings indicate that T cells require macrophages or IL-1 for TSST-1-induced production of IL-2. The roles of lymphokines, including IL-2, in the development of this illness are discussed.

摘要

中毒性休克综合征毒素-1(TSST-1)是从中毒性休克综合征患者体内分离出的金黄色葡萄球菌产生的一种外毒素。我们研究了体外经TSST-1刺激后人淋巴细胞的增殖反应及其白细胞介素2(IL-2)的产生。人脐血单个核细胞(HCBM)和人外周血单个核细胞(HPBM)在TSST-1刺激下能够增殖。去除T细胞的HPBM对这种毒素仅表现出微弱反应。从TSST-1刺激的HPBM培养上清液中获得了一种分子量为15 - 18 kD的IL-2样因子。该因子可被CTLL-2细胞吸收,但不能被去除T细胞的小鼠脾细胞吸收,表明它就是IL-2。HPBM对TSST-1非常敏感:低浓度的TSST-1(36小时刺激中为0.01 ng/ml)和短时间刺激(毒素浓度为10 ng/ml时刺激8小时)就能使HPBM产生大量IL-2。去除T细胞可消除TSST-1诱导的HPBM产生IL-2的能力。经尼龙毛柱分离的T细胞和巨噬细胞重建的细胞培养物在TSST-1刺激下可产生IL-2,此外,巨噬细胞的辅助活性可被一种含白细胞介素1的巨噬细胞衍生因子部分替代。这些发现表明,T细胞在TSST-1诱导产生IL-2过程中需要巨噬细胞或IL-1。本文还讨论了包括IL-2在内的淋巴因子在该疾病发生发展中的作用。

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Toxic-shock syndrome in menstruating women: association with tampon use and Staphylococcus aureus and clinical features in 52 cases.经期女性中毒性休克综合征:与使用卫生棉条及金黄色葡萄球菌的关联及52例临床特征
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Alteration of immune function by staphylococcal pyrogenic exotoxin type C: possible role in toxic-shock syndrome.C型葡萄球菌致热外毒素对免疫功能的改变:在中毒性休克综合征中的可能作用
J Infect Dis. 1983 Mar;147(3):391-8. doi: 10.1093/infdis/147.3.391.
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Induction of human interleukin-1 by a product of Staphylococcus aureus associated with toxic shock syndrome.金黄色葡萄球菌一种与中毒性休克综合征相关的产物诱导人白细胞介素-1的产生。
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