Servet-Delprat C, Vidalain P O, Valentin H, Rabourdin-Combe C
Immunobiologie Fondamentale et Clinique, CERVI-INSERM U503, 21 avenue Tony Garnier, 69007 Lyon, France.
Curr Top Microbiol Immunol. 2003;276:103-23. doi: 10.1007/978-3-662-06508-2_5.
Measles virus (MV) infection induces both an efficient MV-specific immune response and a transient but profound immunosuppression characterised by a panlymphopenia that occasionally results in opportunistic infections responsible for a high rate of mortality in children. On the basis of in vitro studies, the putative roles of dendritic cells (DCs) in MV infection are discussed. (1) DCs could participate in anti-MV innate immunity because MV turns on TNF-related apoptosis-inducing ligand (TRAIL)-mediated DC cytotoxicity. (2) Cross-priming by non-infected DCs might be the route of MV adaptive immune response. (3) After CD40-ligand activation in secondary lymphoid organs, MV-infected DCs could initiate the formation of Warthin-Finkeldey multinucleated giant cells, replicating MV and responsible for in vivo spreading of MV. (4) We review how integrated viral attack of the host immune system also targets DCs: Progress in understanding the immunobiology of MV-infected DCs that could account for MV-induced immunosuppression observed in vivo is presented and their potential role in lymphopenia is underlined. In conclusion, future research directions are proposed.
麻疹病毒（MV）感染既能诱导有效的MV特异性免疫反应，也能导致短暂但严重的免疫抑制，其特征为全淋巴细胞减少，偶尔会引发机会性感染，导致儿童死亡率居高不下。基于体外研究，讨论了树突状细胞（DC）在MV感染中的假定作用。（1）DC可能参与抗MV固有免疫，因为MV开启了肿瘤坏死因子相关凋亡诱导配体（TRAIL）介导的DC细胞毒性。（2）未感染的DC的交叉呈递可能是MV适应性免疫反应的途径。（3）在二级淋巴器官中经CD40配体激活后，感染MV的DC可启动华氏巨细胞的形成，复制MV并导致MV在体内传播。（4）我们综述了宿主免疫系统的整合病毒攻击如何也靶向DC：介绍了在理解感染MV的DC的免疫生物学方面取得的进展，这些进展可以解释在体内观察到的MV诱导的免疫抑制，并强调了它们在淋巴细胞减少中的潜在作用。总之，提出了未来的研究方向。
