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恶性疟原虫的一种变异CD4 T细胞表位通过白细胞介素10介导免疫抑制

Interleukin 10-mediated immunosuppression by a variant CD4 T cell epitope of Plasmodium falciparum.

作者信息

Plebanski M, Flanagan K L, Lee E A, Reece W H, Hart K, Gelder C, Gillespie G, Pinder M, Hill A V

机构信息

Institute of Molecular Medicine, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, United Kingdom.

出版信息

Immunity. 1999 Jun;10(6):651-60. doi: 10.1016/s1074-7613(00)80064-3.

Abstract

The immunodominant CD4 T cell epitope region, Th2R, of the circumsporozoite protein of Plasmodium falciparum is highly polymorphic. Such variation might be utilized by the parasite to escape from or interfere with CD4 T cell effector functions. Here, we show that costimulation with naturally occurring altered peptide ligands (APL) can induce a rapid change from IFNgamma production to the immunosuppressive mediator interleukin 10 (IL-10). This mechanism may contribute to the low levels of T cell responses observed to this pathogen in malaria-endemic areas.

摘要

恶性疟原虫环子孢子蛋白的免疫显性CD4 T细胞表位区Th2R具有高度多态性。寄生虫可能利用这种变异来逃避或干扰CD4 T细胞效应功能。在此,我们表明,与天然存在的改变肽配体(APL)共刺激可诱导从产生干扰素γ迅速转变为产生免疫抑制介质白细胞介素10(IL-10)。这一机制可能导致在疟疾流行地区观察到针对该病原体的T细胞反应水平较低。

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