van Kooyk Yvette, Geijtenbeek Teunis B H
Department of Molecular Cell Biology and Immunology Vrije Universiteit Medical Center Amsterdam, v.d. Boechorststraat 7, 1081 BT Amsterdam, The Netherlands.
Nat Rev Immunol. 2003 Sep;3(9):697-709. doi: 10.1038/nri1182.
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.
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。
