Measles virus interacts with human SLAM receptor on dendritic cells to cause immuno suppression
Measles virus interacts with human SLAM receptor on dendritic cells to cause immuno suppression
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DOI：
10.1016/j.virol.2004.03.011
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发表时间：
2004-06-01
期刊：
影响因子：
3.7
通讯作者：
Oldstone, MBA
中科院分区：
文献类型：
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作者：
Hahm, B;Arbour, N;Oldstone, MBA
麻疹病毒（MV）感染树突状细胞（DC）导致免疫抑制。人DC表达两种MV受体：CD 46和人信号淋巴细胞活化分子（hSLAM）;因此，单独发挥的作用尚不清楚。由于野生型（wt）MV优先使用hSLAM受体，我们通过在DC上产生表达hSLAM的转基因（tg）小鼠，剖析了MV-DC相互作用的分子基础和通过hSLAM受体产生的免疫抑制。感染野生型MV后，表达hSLAM受体的海洋脾脏DC在其表面上具有较少的B7-1、B7-2、CD 40、MHC I类和MHC II类分子，并且当与未感染的DC相比时显示出增加的凋亡率。此外，MV感染的DC不能刺激同种异体T细胞并抑制促分裂原依赖性T细胞增殖。MV感染的DC抑制T细胞增殖不需要来自T细胞的人SLAM、干扰素α/β受体、肿瘤坏死因子-α、以及抗肿瘤毒素-α或β的单独表达。(C)2004爱思唯尔公司All rights reserved.
Measles virus (MV) infects dendritic cells (DCs) resulting in immunosuppression. Human DCs express two MV receptors: CD46 and human signaling lymphocyte activation molecule (hSLAM); thus, the role played by either alone is unclear. Because wild-type (wt) MV uses hSLAM receptor preferentially, we dissected the molecular basis of MV-DC interaction and resultant immunosuppression through the hSLAM receptor by creating transgenic (tg) mice expressing hSLAM on DCs. After infection with wt MV, marine splenic DCs expressing hSLAM receptor had less B7-1, B7-2, CD40, MHC class I, and MHC class II molecules on their surfaces and displayed an increased rate of apoptosis when compared to uninfected DCs. Further, MV-infected DCs failed to stimulate allogeneic T cells and inhibited mitogen-dependent T-cell proliferation. Individual expression of human SLAM, interferon alpha/beta receptor, tumor necrosis factor-a, and lymphotoxin-a or beta from T cells was not required for MV-infected DCs to inhibit the proliferation of T cells. (C) 2004 Elsevier Inc. All rights reserved.