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TCRαβ +  CD4 − CD8 − NK −  double negative T cells (DN T cells) can act as regulatory T cells to inhibit allograft rejection and autoimmunity. Their role in graft-versus-host disease and mechanisms of suppression remain elusive. In this study, we demonstrate that DN T cells can inhibit CD4 +  T cell-mediated GVHD in a semi-allogeneic model of bone marrow transplantation. Furthermore, we present evidence of a novel autocrine IFNγ signaling pathway in Fas-deficient C57BL/6. lpr  (B6. lpr ) DN T cells. B6. lpr  DN T cells lacking IFNγ or its receptor were impaired in their ability to suppress syngeneic CD4 +  T cells responding to alloantigen stimulation both  in vitro  and  in vivo . Autocrine IFNγ signaling was required for sustained B6. lpr  DN T cell IFNγ secretion  in vivo  and for upregulation of surface Fas ligand expression during TCR stimulation. Fas ligand (FasL) expression by B6. lpr  DN T cells permitted lysis of activated CD4 +  T cells and was required for suppression of GVHD. Collectively, our data indicate that DN T cells can inhibit GVHD and that IFNγ plays a critical autocrine role in controlling the regulatory function of B6. lpr  DN T cells.

Autocrine IFNγ Controls the Regulatory Function of Lymphoproliferative Double Negative T Cells