期刊名称:Proceedings of the National Academy of Sciences
印刷版ISSN:0027-8424
电子版ISSN:1091-6490
出版年度:2009
卷号:106
期号:13
页码:5300-5305
DOI:10.1073/pnas.0808851106
语种:English
出版社:The National Academy of Sciences of the United States of America
摘要: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 naive CD8+ T cells. We also show that antiviral CD8+ T cell responses are enhanced by administration of a {beta}2 (but not {beta}1 or {alpha}) 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 {beta}-blockers, one of the most widely prescribed classes of drugs.