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Blood, 21 May 2009, Vol. 113, No. 21, pp. 5134-5143. Prepublished online as a Blood First Edition Paper on March 17, 2009; DOI 10.1182/blood-2008-11-190769. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-11-190769v1 113/21/5134    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dimitrov, S. Articles by Lange, T. Search for Related Content PubMed PubMed Citation Articles by Dimitrov, S. Articles by Lange, T. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Cortisol and epinephrine control opposing circadian rhythms in T cell subsets Stoyan Dimitrov1, Christian Benedict1, Dennis Heutling2, Jürgen Westermann3, Jan Born1, and Tanja Lange1,2 Departments of 1 Neuroendocrinology, 2 Internal Medicine, and 3 Anatomy, University of Lübeck, Lübeck, Germany Pronounced circadian rhythms in numbers of circulating T cells reflect a systemic control of adaptive immunity whose mechanisms are obscure. Here, we show that circadian variations in T cell subpopulations in human blood are differentially regulated via release of cortisol and catecholamines. Within the CD4+ and CD8+ T cell subsets, naive cells show pronounced circadian rhythms with a daytime nadir, whereas (terminally differentiated) effector CD8+ T cell counts peak during daytime. Naive T cells were negatively correlated with cortisol rhythms, decreased after low-dose cortisol infusion, and showed highest expression of CXCR4, which was up-regulated by cortisol. Effector CD8+ T cells were positively correlated with epinephrine rhythms, increased after low-dose epinephrine infusion, and showed highest expression of β-adrenergic and fractalkine receptors (CX3CR1). Daytime increases in cortisol via CXCR4 probably act to redistribute naive T cells to bone marrow, whereas daytime increases in catecholamines via β-adrenoceptors and, possibly, a suppression of fractalkine signaling promote mobilization of effector CD8+ T cells from the marginal pool. Thus, activation of the major stress hormones during daytime favor immediate effector defense but diminish capabilities for initiating adaptive immune responses. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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