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 Blood, 21 May 2009, Vol. 113, No. 21, pp. 5202-5205.
Prepublished online as a Blood First Edition Paper on March 26, 2009; DOI 10.1182/blood-2008-09-181255.

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Submitted September 30, 2008
Accepted February 26, 2009

Reduction of T cell-derived ghrelin enhances proinflammatory cytokine expression: implications for age-associated increases in inflammation

Vishwa Deep Dixit, Hyunwon Yang, Anthony Cooper-Jenkins, Banabihari B. Giri, Kalpesh Patel, and Dennis D. Taub*

Laboratory of Immunology, National Institute on Aging-Intramural Research Program, National Institutes of Health, Baltimore, MD, United States

* Corresponding author; email: taubd{at}grc.nia.nih.gov.

Ghrelin (Grln) is a peptide hormone that is predominantly produced in the stomach and stimulates appetite and induces Growth Hormone (GH) release. We have previously reported that ghrelin is also expressed in T cells and exerts pro-thymic and anti-inflammatory effects. However, the biological relevance of T-cell derived ghrelin remains to be determined. Here, we report that acylated-bioactive ghrelin is expressed in human T cells and preferentially segregates within the lipid raft domains upon TCR ligation. The RNA interference (RNAi) mediated down regulation of ghrelin in primary human T cells activates IkB, increases Th1 cytokines and IL-17 secretion. Ghrelin expression declines with increasing age in spleen and T cells and exogenous ghrelin administration in old mice reduces pro-inflammatory cytokines. These findings demonstrate that ghrelin functions in an autocrine and paracrine capacity to regulate pro-inflammatory cytokine expression in human and murine T cells and may contribute in regulating 'inflamm-aging'.


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H. Yang, Y.-H. Youm, B. Vandanmagsar, J. Rood, K. G. Kumar, A. A. Butler, and V. D. Dixit
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[Abstract] [Full Text] [PDF]


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