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树突状细胞特异性细胞间黏附分子-3结合非整合素(DC-SIGN):病原体的逃逸机制

DC-SIGN: escape mechanism for pathogens.

作者信息

van Kooyk Yvette, Geijtenbeek Teunis B H

机构信息

Department of Molecular Cell Biology and Immunology Vrije Universiteit Medical Center Amsterdam, v.d. Boechorststraat 7, 1081 BT Amsterdam, The Netherlands.

出版信息

Nat Rev Immunol. 2003 Sep;3(9):697-709. doi: 10.1038/nri1182.

Abstract

Dendritic cells (DCs) are crucial in the defence against pathogens. Invading pathogens are recognized by Toll-like receptors (TLRs) and receptors such as C-type lectins expressed on the surface of DCs. However, it is becoming evident that some pathogens, including viruses, such as HIV-1, and non-viral pathogens, such as Mycobacterium tuberculosis, subvert DC functions to escape immune surveillance by targeting the C-type lectin DC-SIGN (DC-specific intercellular adhesion molecule-grabbing nonintegrin). Notably, these pathogens misuse DC-SIGN by distinct mechanisms that either circumvent antigen processing or alter TLR-mediated signalling, skewing T-cell responses. This implies that adaptation of pathogens to target DC-SIGN might support pathogen survival.

摘要

树突状细胞(DCs)在抵御病原体方面至关重要。入侵的病原体可被Toll样受体(TLRs)以及DCs表面表达的如C型凝集素等受体识别。然而,越来越明显的是,一些病原体,包括病毒(如HIV-1)和非病毒病原体(如结核分枝杆菌),通过靶向C型凝集素DC-SIGN(DC特异性细胞间粘附分子捕获非整合素)来颠覆DC功能,从而逃避免疫监视。值得注意的是,这些病原体通过不同机制滥用DC-SIGN,这些机制要么规避抗原加工,要么改变TLR介导的信号传导,从而使T细胞反应发生偏差。这意味着病原体对DC-SIGN的靶向适应可能有助于病原体存活。

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