Seya T
Interitance and Variation' in PRESTO, Research Development Cooperation of Japan (JRDC), Kyoto, Japan.
Int J Hematol. 1996 Aug;64(2):101-9. doi: 10.1016/0925-5710(96)00476-8.
During measles virus (MV) infection, lymphopenia and immune suppression are observed in humans, yet the mechanisms underlying these effects remain unknown except that membrane cofactor protein (MCP, CD46) acts as a receptor for MV, accelerating entry of the virus into host cells. CD46 is a complement regulator, the role of which is to protect host cells from the autologous complement system. Thus, it encompasses complement-related and MV-mediated immune modulation. In this review, I discuss the structural and functional differences between CD46 on lymphocytes and on granulocytes, which partly explain the higher susceptibility of lymphocytes to MV than other blood cells to clarify the mechanisms of MV-mediated lymphopenia and immune suppression, and help resolve the T cell immunity dysfunction secondary to virus infection including HIV.
在麻疹病毒（MV）感染期间，人类会出现淋巴细胞减少和免疫抑制现象，但除了膜辅因子蛋白（MCP，CD46）作为MV的受体，加速病毒进入宿主细胞外，这些效应背后的机制仍不清楚。CD46是一种补体调节因子，其作用是保护宿主细胞免受自身补体系统的攻击。因此，它涉及补体相关和MV介导的免疫调节。在这篇综述中，我讨论了淋巴细胞和粒细胞上CD46的结构和功能差异，这部分解释了淋巴细胞比其他血细胞对MV更易感的原因，以阐明MV介导的淋巴细胞减少和免疫抑制机制，并有助于解决包括HIV在内的病毒感染继发的T细胞免疫功能障碍。
