McDermott Daniel S, Weiss Kayla A, Knudson Cory J, Varga Steven M
Interdisciplinary Graduate Program in Immunology, 51 Newton Road, 3-532 Bowen Science Building, University of Iowa, Iowa City, IA 52242, USA.
Future Virol. 2011 Aug;6(8):963-973. doi: 10.2217/fvl.11.62.
Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract disease in young children. Premature infants, immunocompromised individuals and the elderly exhibit the highest risk for the development of severe RSV-induced disease. Murine studies demonstrate that CD8 T cells mediate RSV clearance from the lungs. Murine studies also indicate that the host immune response contributes to RSV-induced morbidity as T-cell depletion prevents the development of disease despite sustained viral replication. Dendritic cells (DCs) play a central role in the induction of the RSV-specific adaptive immune response. Following RSV infection, lung-resident DCs acquire viral antigens, migrate to the lung-draining lymph nodes and initiate the T-cell response. This article focuses on data generated from both in vitro DC infection studies and RSV mouse models that together have advanced our understanding of how RSV infection modulates DC function and the subsequent impact on the adaptive immune response.
呼吸道合胞病毒（RSV）是幼儿下呼吸道疾病的主要病因。早产儿、免疫功能低下者和老年人患严重RSV诱发疾病的风险最高。小鼠研究表明，CD8 T细胞介导肺部RSV的清除。小鼠研究还表明，宿主免疫反应会导致RSV诱发的发病，因为尽管病毒持续复制，但T细胞耗竭可预防疾病的发展。树突状细胞（DCs）在RSV特异性适应性免疫反应的诱导中起核心作用。RSV感染后，肺驻留DCs获取病毒抗原，迁移至引流肺的淋巴结并启动T细胞反应。本文重点关注体外DC感染研究和RSV小鼠模型产生的数据，这些数据共同加深了我们对RSV感染如何调节DC功能以及对适应性免疫反应的后续影响的理解。
