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BioMed Research International
Volume 2013 (2013), Article ID 160859, 11 pages
http://dx.doi.org/10.1155/2013/160859
Research Article

Chronic Heat Stress Inhibits Immune Responses to H5N1 Vaccination through Regulating CD4+CD25+Foxp3+ Tregs

1Key Laboratory of Zoonosis of Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan, West Road, Beijing 100193, China
2Institute of Laboratory Animal Science, Chinese Academy of Medical Science, Beijing 100021, China
3State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100193, China
4Zhongmu Institutes of China Animal Husbandry Group, No. 156 Beiqing Road, Haidian District, Beijing 100095, China

Received 9 July 2013; Accepted 4 August 2013

Academic Editor: Hajime Hisaeda

Copyright © 2013 Di Meng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Chronic heat stress (CHS) is known to have negative impacts on the immune responses in animals and increases their susceptibility to infections including the highly pathogenic avian influenza virus H5N1. However, the role of regulatory T cells (Tregs) in CHS immunosuppression remains largely undefined. In this study, we demonstrated a novel mechanism by which CHS suppressed both Th1 and Th2 immune responses and dramatically decreased the protective efficacy of the formalin-inactivated H5N1 vaccine against H5N1 influenza virus infection. This suppression was found to be associated with the induced generation of CD4+CD25+FoxP3+ Tregs and the increased secretions of IL-10 and TGF-β in CD4+ T cells. Adoptive transfer of the induced Tregs also suppressed the protective efficacy of formalin-inactivated H5N1 virus immunization. Collectively, this study identifies a novel mechanism of CHS immunosuppression mediated by regulating CD4+CD25+Foxp3+ Tregs.