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    J Immunol. 2001 Nov 15;167(10):5527-30.

    NKG2D receptors induced by IL-15 costimulate CD28-negative effector CTL in the tissue microenvironment.

    Roberts AI, Lee L, Schwarz E, Groh V, Spies T, Ebert EC, Jabri B.

    Source

    Department of Medicine, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ 08903, USA.

    Abstract

    Unlike primary T cells in lymph nodes, effector CD8(+) CTL in tissues do not express the costimulatory receptor CD28. We report that NKG2D, the receptor for stress-induced MICA and MICB molecules expressed in the intestine, serves as a potent costimulatory receptor for CTL freshly isolated from the human intestinal epithelium. Expression and function of NKG2D are selectively up-regulated by the cytokine IL-15, which is released by the inflamed intestinal epithelium. These findings identify a novel CTL costimulatory pathway regulated by IL-15 and suggest that tissues can fine-tune the activation of effector T cells based on the presence or absence of stress and inflammation. Uncontrolled secretion of IL-15 could lead to excessive induction of NKG2D and thus contribute to the development of autoimmune disease by facilitating the activation of autoreactive T cells.

    PMID:
    11698420
    [PubMed - indexed for MEDLINE]
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