病毒诱导的CD1d1介导的抗原呈递抑制：p38和ERK的相互调节

Virus-induced inhibition of CD1d1-mediated antigen presentation: reciprocal regulation by p38 and ERK.

作者信息

Renukaradhya Gourapura J, Webb Tonya J Roberts, Khan Masood A, Lin Yin Ling, Du Wenjun, Gervay-Hague Jacquelyn, Brutkiewicz Randy R

机构信息

Department of Microbiology and Immunology, Indiana University School of Medicine, Walther Oncology Center, Indianapolis, IN 46202, USA.

出版信息

J Immunol. 2005 Oct 1;175(7):4301-8. doi: 10.4049/jimmunol.175.7.4301.

DOI:10.4049/jimmunol.175.7.4301

PMID:16177070

Abstract

A critical component of the host's innate immune response involves lipid Ag presentation by CD1d molecules to NK T cells. In this study we used murine CD1d1-transfected L (L-CD1) cells to study the effect of viruses on CD1d-mediated Ag presentation to NKT cells and found that an infection with vesicular stomatitis and vaccinia (but not lymphocytic choriomeningitis) virus inhibited murine CD1d1-mediated Ag presentation. This was under the reciprocal control of the MAPKs, p38 and ERK, and was due to changes in the intracellular trafficking of CD1d1. The reciprocal regulation of CD1d1-mediated Ag presentation by MAPK suggests that the targeting of these pathways is a novel means of immune evasion by viruses.

摘要

宿主固有免疫反应的一个关键组成部分涉及CD1d分子将脂质抗原呈递给自然杀伤T细胞。在本研究中，我们使用转染了鼠CD1d1的L（L-CD1）细胞来研究病毒对CD1d介导的抗原呈递给自然杀伤T细胞的影响，发现感染水疱性口炎病毒和痘苗病毒（但不包括淋巴细胞性脉络丛脑膜炎病毒）会抑制鼠CD1d1介导的抗原呈递。这受丝裂原活化蛋白激酶p38和细胞外信号调节激酶的相互调控，并且是由于CD1d1细胞内运输的变化所致。丝裂原活化蛋白激酶对CD1d1介导的抗原呈递的相互调节表明，靶向这些信号通路是病毒逃避免疫的一种新方式。