Avota Elita, Schneider-Schaulies Sibylle
Institute for Virology and Immunobiology, University of Wuerzburg, Wuerzburg, Germany.
Cell Physiol Biochem. 2014;34(1):20-6. doi: 10.1159/000362981. Epub 2014 Jun 16.
Measles virus (MV) efficiently causes generalized immunosuppression which accounts to a major extent for cases of measles-asscociated severe morbidity and mortality. MV infections alter many functions of antigen presenting cells (APC) (dendritic cells (DCs)) and lymphocytes, yet many molecular targets of the virus remain poorly defined. Cellular interactions and effector functions of DCs and lymphocytes are regulated by surface receptors. Associating with other proteins involved in cell signaling, receptors form part of receptosomes that respond to and transmit external signals through dynamic interctions with the cytoskeleton. Alterations in the composition and metabolism of membrane sphingolipids have a substantial impact on both processes. In this review we focus on the regulation of sphingomyelinase activity and ceramide release in cells exposed to MV and discuss the immunosuppressive role of sphingomyelin breakdown induced by MV.
麻疹病毒（MV）可有效导致全身性免疫抑制，这在很大程度上是麻疹相关严重发病和死亡病例的原因。MV感染会改变抗原呈递细胞（APC）（树突状细胞（DCs））和淋巴细胞的许多功能，但该病毒的许多分子靶点仍不清楚。DCs和淋巴细胞的细胞间相互作用和效应功能由表面受体调节。受体与参与细胞信号传导的其他蛋白质结合，形成受体体的一部分，通过与细胞骨架的动态相互作用来响应和传递外部信号。膜鞘脂的组成和代谢变化对这两个过程都有重大影响。在本综述中，我们重点关注暴露于MV的细胞中鞘磷脂酶活性和神经酰胺释放的调节，并讨论MV诱导的鞘磷脂分解的免疫抑制作用。
