Vaccinia virus infection induces dendritic cell maturation but inhibits antigen presentation by MHC class II

被引:36
|
作者
Yao, Yongxue
Li, Ping
Singh, Pratibha
Thiele, Allison T.
Wilkes, David S.
Renukaradhya, Gourapura J.
Brutkiewicz, Randy R.
Travers, Jeffrey B.
Luker, Gary D.
Hong, Soon-Cheol
Blum, Janice S.
Chang, Cheong-Hee [1 ]
机构
[1] Indiana Univ, Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA
[2] Indiana Univ, Sch Med, Walther Oncol Ctr, Indianapolis, IN 46202 USA
[3] Indiana Univ, Dept Med, Indianapolis, IN 46202 USA
[4] Indiana Univ, Sch Med, Dept Dermatol, Indianapolis, IN 46202 USA
[5] Indiana Univ, Sch Med, HB Wells Ctr Pediat Res, Indianapolis, IN 46202 USA
[6] Univ Michigan, Sch Med, Dept Radiol, Ann Arbor, MI 48109 USA
[7] Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA
关键词
vaccinia virus; dendritic cell; MHC class II; gene regulation; Cytokines; type I interferon; innate immunity;
D O I
10.1016/j.cellimm.2007.06.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Vaccinia virus (W) infection is known to inhibit dendritic cells (DC) functions in vitro. Paradoxically, VV is also highly immunogenic and thus has been used as a vaccine. In the present study, we investigated the effects of an in vivo VV infection on DC function by focusing on early innate immunity. Our data indicated that DC are activated upon in vivo VV infection of mice. Splenic DC from W-infected mice expressed elevated levels of MHC class I and co-stimulatory molecules on their cell surface and exhibited the enhanced potential to produce cytokines upon LPS stimulation. DC from W-infected mice also expressed a high level of interferon-P. However, a VV infection resulted in the down-regulation of MHC class II expression and the impairment of antigen presentation to CD4 T cells by DC. Thus, during the early stage of a VV infection, although DC are impaired in some of the critical antigen presentation functions, they can promote innate immune defenses against viral infection. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:92 / 102
页数:11
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