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    Nat Immunol. 2006 Jul;7(7):755-62. Epub 2006 May 28.

    Fas-ligand-mediated paracrine T cell regulation by the receptor NKG2D in tumor immunity.

    Groh V, Smythe K, Dai Z, Spies T.

    Source

    Fred Hutchinson Cancer Research Center, Clinical Research Division, Seattle, Washington 98109, USA.

    Erratum in

    • Nat Immunol. 2006 Sep;7(9):1004.

    Abstract

    Tumor-associated ligands of the activating NKG2D receptor can effectively stimulate T cell responses at early but not late stages of tumor growth. In late-stage human tumor settings, we observed MIC-driven proliferation of NKG2D(+)CD4(+) T cells that produced the cytokine Fas ligand (FasL) as a result of NKG2D costimulation but were themselves protected from Fas-mediated growth arrest. In contrast, FasL suppressed proliferation of T cells in vitro that did not receive NKG2D costimulation. Similar observations with normal peripheral blood NKG2D(+)CD8(+) T cells demonstrated unrecognized NKG2D-mediated immune functions, whereby FasL release promotes tumor cell death and NKG2D costimulation prolongs T cell survival. These effects, beneficial in conditions of limited NKG2D ligand expression, may be counterweighed when massive expression and shedding of MIC occurs, such as in some late-stage tumors, that causes sustained NKG2D costimulation and population expansion of immunosuppressive T cells.

    PMID:
    16732291
    [PubMed - indexed for MEDLINE]

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