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对葡萄球菌超抗原的免疫反应。

Immune response to staphylococcal superantigens.

作者信息

Krakauer T

机构信息

Department of Immunology and Molecular Biology, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702-5011, USA.

出版信息

Immunol Res. 1999;20(2):163-73. doi: 10.1007/BF02786471.

Abstract

Staphylococcal exotoxins, staphylococcal enterotoxins A-E (SEA-SEE), and toxic shock syndrome toxin- (TSST-1) are potent activators of the immune system and cause a variety of diseases in humans, ranging from food poisoning to shock. These toxins are called superantigens because of their ability to polyclonally activate T cells at picromolar concentrations. Superantigens bind to both MHC class II molecules and specific Vbeta regions of the T cell receptor, leading to the activation of both antigen-presenting cells and T lymphocytes. These interactions lead to excessive production of proinflammatory cytokines and T cell proliferation, causing clinical symptoms that include fever, hypotension, and shock. Recent studies suggest that staphylococcal superantigens may also be involved in the pathogenesis of arthritis and other autoimmune disorders. This review summarizes the in vitro and in vivo effects of staphylococcal enterotoxins and TSST-1, recent progress with the use of transgenic knockout mice to identify key mediators and receptors involved in superantigen-induced shock, and therapeutic agents to mitigate the toxic effects of staphylococcal superantigens.

摘要

葡萄球菌外毒素、葡萄球菌肠毒素A-E(SEA-SEE)和中毒性休克综合征毒素-1(TSST-1)是免疫系统的强效激活剂,可导致人类多种疾病,从食物中毒到休克不等。这些毒素被称为超抗原,因为它们能够在皮摩尔浓度下多克隆激活T细胞。超抗原与MHC II类分子和T细胞受体的特定Vβ区域结合,导致抗原呈递细胞和T淋巴细胞均被激活。这些相互作用导致促炎细胞因子过度产生和T细胞增殖,引起包括发热、低血压和休克在内的临床症状。最近的研究表明,葡萄球菌超抗原也可能参与关节炎和其他自身免疫性疾病的发病机制。本综述总结了葡萄球菌肠毒素和TSST-1的体外和体内作用、利用转基因敲除小鼠鉴定超抗原诱导休克中关键介质和受体的最新进展,以及减轻葡萄球菌超抗原毒性作用的治疗药物。

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