期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 25, 期 2, 页码 340-348出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2010.10.016
关键词
Cytotoxic T cells; Viral infection; Social stress; Corticosterone; Dendritic cells
资金
- German Research Foundation, Research Group [FOR 751, B1, GR 1517/6-1, EN 814/1-2]
Chronic stress is suspected to increase the susceptibility to infections but experimental evidence from physiological stress models is scarce. We examined the effects of chronic social stress on virus-specific CTL responses in mice after infection with lymphocytic choriomeningitis virus (LCMV). Mice subjected to social stress on six consecutive days prior to infection showed a significant reduction of IFN-gamma producing TCD8+ splenocytes and markedly lowered plasma concentrations of IFN-gamma. In contrast, the generation of LCMV-specific CTL responses was not altered in mice undergoing the same stress procedure concurrently with infection. Furthermore, stress exposure 6 days before and additional 3 days after LCMV infection profoundly reduced the expansion of TCD8+ cells in the spleen, due to diminished in vivo proliferation. Pharmacological blockade of glucocorticoid receptors completely abrogated the stress-associated decline of TCD8+ expansion. Stressed mice showed a significantly reduced expression of the early T-cell activation marker CD69 as well as impaired in vitro cytokine secretion of IFN-gamma and IL-2. Additionally, social stress led to an altered migration capacity of TCD8+ cells as demonstrated by adoptive T cell transfer experiments. Taken together, this study shows that chronic social stress fundamentally suppresses the functional capacities of T cells during a viral infection. (C) 2010 Elsevier Inc. All rights reserved.
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