Coxsackievirus B3 Inhibits Antigen Presentation In Vivo, Exerting a Profound and Selective Effect on the MHC Class I Pathway

PLoS Pathogens

Ralph Feuer¹  Stephanie Harkins²  Claudia T. Flynn²  Christopher C. Kemball²  Jason K. Whitmire²  J. Lindsay Whitton² 

[1] Department of Biology, San Diego State University, San Diego, California, United States of America;Department of Immunology and Microbial Science, SP30-2110, The Scripps Research Institute, La Jolla, California, United States of America

关键词: T cells;    Cytotoxic T cells;    Memory T cells;    Antigen presentation;    Major histocompatibility complex;    Spleen;    Cell cycle;    cell division;    Genetically modified animals;   

DOI  :  10.1371/journal.ppat.1000618

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

Many viruses encode proteins whose major function is to evade or disable the host T cell response. Nevertheless, most viruses are readily detected by host T cells, and induce relatively strong T cell responses. Herein, we employ transgenic CD4+ and CD8+ T cells as sensors to evaluate in vitro and in vivo antigen presentation by coxsackievirus B3 (CVB3), and we show that this virus almost completely inhibits antigen presentation via the MHC class I pathway, thereby evading CD8+ T cell immunity. In contrast, the presentation of CVB3-encoded MHC class II epitopes is relatively unencumbered, and CVB3 induces in vivo CD4+ T cell responses that are, by several criteria, phenotypically normal. The cells display an effector phenotype and mature into multi-functional CVB3-specific memory CD4+ T cells that expand dramatically following challenge infection and rapidly differentiate into secondary effector cells capable of secreting multiple cytokines. Our findings have implications for the efficiency of antigen cross-presentation during coxsackievirus infection.

【 授权许可】

CC BY