Sympathetic nervous system control of anti-influenza CD8+T cell responses

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Abstract
Despite the longstanding appreciation of communication between the nervous and the immune systems, the nature and significance of these interactions to immunity remain enigmatic. Here, we show that 6-hydroxydopamine-mediated ablation of the mouse peripheral sympathetic nervous system increases primary CD8+T cell responses to viral and cellular antigens presented by direct priming or cross-priming. The sympathetic nervous system also suppresses antiviral CD4+T cell responses, but this is not required for suppressing CD8+T cell responses. Adoptive transfer experiments indicate that enhanced CD8+responses do not result from permanent alterations in CD8+T cell function in sympathectomized mice. Rather, additional findings suggest that the sympathetic nervous system tempers the capacity of antigen-presenting cells to activate naïve CD8+T cells. We also show that antiviral CD8+T cell responses are enhanced by administration of a β2(but not β1or α) adrenergic antagonist. These findings demonstrate a critical role for the sympathetic nervous system in limiting CD8+T cell responses and indicate that CD8+T cell responses may be altered in patients using β-blockers, one of the most widely prescribed classes of drugs.

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