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作为MHC II类依赖性T细胞抗原受体探针的促有丝分裂毒素

Mitogenic toxins as MHC class II-dependent probes for T cell antigen receptors.

作者信息

Fleischer B, Mittrücker H W, Metzroth B, Braun M, Hartwig U

机构信息

I. Department of Medicine, University of Mainz, Germany.

出版信息

Behring Inst Mitt. 1991 Feb(88):170-6.

PMID:2049035
Abstract

The enterotoxins produced by Staphylococcus aureus (SE) are prototypes of a group of microbial exoproteins that share a potent mitogenic activity for T lymphocytes of several species. These exoproteins use a very effective novel mechanism of T lymphocyte stimulation. For stimulation of all types of T cells (CD4+, CD8+ as well as gamma delta TCR+) the presence of allogeneic or xenogeneic MHC class II molecules on accessory or target cells is required. This requirement is reflected by a selective binding of the toxins to MHC class II molecules. The toxins stimulate preferentially but not exclusively alpha beta TCR+ T cells carrying certain TCR V beta s. A current model suggests that the toxins are functionally bivalent molecules, crosslinking variable parts of the TCR with MHC class II molecules on the accessory or target cells. Of all T cell mitogens the toxins thus most closely simulate T cell recognition of specific antigen. The differential pattern of reactivity of human and murine T cells with various toxins suggests that the toxins have been adapted to the host's immune system in evolution.

摘要

金黄色葡萄球菌(SE)产生的肠毒素是一类微生物外毒素的原型,这类外毒素对多种物种的T淋巴细胞具有强大的促有丝分裂活性。这些外毒素采用了一种非常有效的新型T淋巴细胞刺激机制。为了刺激所有类型的T细胞(CD4+、CD8+以及γδTCR+),辅助细胞或靶细胞上需要存在同种异体或异种MHC II类分子。毒素与MHC II类分子的选择性结合反映了这一需求。毒素优先但并非唯一地刺激携带某些TCR Vβs的αβTCR+ T细胞。目前的模型表明,毒素是功能上的二价分子,将TCR的可变部分与辅助细胞或靶细胞上的MHC II类分子交联。因此,在所有T细胞促有丝分裂原中,毒素最接近模拟T细胞对特定抗原的识别。人类和小鼠T细胞对各种毒素的不同反应模式表明,这些毒素在进化过程中已适应宿主的免疫系统。

相似文献

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Mitogenic toxins as MHC class II-dependent probes for T cell antigen receptors.作为MHC II类依赖性T细胞抗原受体探针的促有丝分裂毒素
Behring Inst Mitt. 1991 Feb(88):170-6.
2
An evolutionary conserved mechanism of T cell activation by microbial toxins. Evidence for different affinities of T cell receptor-toxin interaction.微生物毒素激活T细胞的一种进化保守机制。T细胞受体与毒素相互作用不同亲和力的证据。
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Activation of MHC class I-restricted CD8+ CTL by microbial T cell mitogens. Dependence upon MHC class II expression of the target cells and V beta usage of the responder T cells.微生物T细胞促细胞分裂剂对MHC I类限制性CD8+细胞毒性T淋巴细胞的激活作用。对靶细胞MHC II类表达及应答T细胞Vβ使用情况的依赖性。
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Bacterial proteins that mediate the association of a defined subset of T cell receptor:CD4 complexes with class II MHC.介导特定子集的T细胞受体:CD4复合物与II类主要组织相容性复合体结合的细菌蛋白。
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Intercellular adhesion molecule-1 and leukocyte function-associated antigen-3 provide costimulation for superantigen-induced T lymphocyte proliferation in the absence of a specific presenting molecule.细胞间黏附分子-1和白细胞功能相关抗原-3在缺乏特异性呈递分子的情况下为超抗原诱导的T淋巴细胞增殖提供共刺激。
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Use of bispecific heteroconjugated antibodies (anti-T cell antigen receptor x anti-MHC class II) to study activation of T cells with a full length or truncated antigen receptor zeta-chain.使用双特异性异源缀合抗体(抗T细胞抗原受体x抗MHC II类)研究具有全长或截短抗原受体ζ链的T细胞激活。
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Residues of the variable region of the T-cell-receptor beta-chain that interact with S. aureus toxin superantigens.与金黄色葡萄球菌毒素超抗原相互作用的T细胞受体β链可变区残基。
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Clonal analysis of human T cell activation by the Mycoplasma arthritidis mitogen (MAS).关节炎支原体促细胞分裂剂(MAS)对人T细胞激活的克隆分析。
Eur J Immunol. 1988 Nov;18(11):1733-7. doi: 10.1002/eji.1830181112.

引用本文的文献

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Food poisoning and Staphylococcus aureus enterotoxins.食物中毒与金黄色葡萄球菌肠毒素。
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2
Differential induction of tumor necrosis factor alpha in murine and human leukocytes by Mycoplasma arthritidis-derived superantigen.
Infect Immun. 1994 Feb;62(2):462-7. doi: 10.1128/iai.62.2.462-467.1994.