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CD56 Marks an Effector T Cell Subset in the Human Intestine¹

Cedars-Sinai Inflammatory Bowel Disease Center, Los Angeles, CA 90048

T cells are key mediators of intestinal immunity, and specific T cell subsets can have differing immunoregulatory roles in animal models of mucosal inflammation. In this study, we describe human CD56⁺ T cells as a morphologically distinct population expressing a mature, nonproliferative phenotype that is frequent in the gut. Enhanced potential for IFN- and TNF synthesis suggested a proinflammatory function, and we directly demonstrate effector function mediated by direct T-T interaction with responder cells in vitro. CD56⁺ T cells from peripheral blood responded to the gut-related CD2 signal, and were necessary for effective CD2-mediated proliferation of peripheral blood CD56^– T cells. Our findings associate CD56⁺ T cells with the intestinal immune compartment and suggest a putative effector function in human mucosal immunity.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by National Institutes of Health Grants F32DK10139 (to O.C.) and R01DK57328/R01DK43211 (to S.R.T.).

² Address correspondence and reprint requests to Dr. Stephan R. Targan, Cedars-Sinai Inflammatory Bowel Disease Center, 8700 Beverly Boulevard, Suite D4063, Los Angeles, CA 90048. E-mail: targans{at}cshs.org

³ Abbreviations used in this paper: IBD, inflammatory bowel disease; CD, Crohn’s disease; UC, ulcerative colitis; LPMC, mononuclear cells from the intestinal lamina propria; LP, lamina propria; MLN, mesenteric lymph node; LN, lymph node; PB, peripheral blood; P/I, PMA and ionomycin; E:R, effector:responder.

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