Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
922672 | Brain, Behavior, and Immunity | 2011 | 9 Pages |
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-γ producing TCD8+TCD8+ splenocytes and markedly lowered plasma concentrations of IFN-γ. 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+TCD8+ cells in the spleen, due to diminished in vivo proliferation. Pharmacological blockade of glucocorticoid receptors completely abrogated the stress-associated decline of TCD8+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-γ and IL-2. Additionally, social stress led to an altered migration capacity of TCD8+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.