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9V
2 T Cells by NKG2D1
* Institut für Virologie und Immunobiologie,
Medizinische Poliklinik, Julius-Maximilians Universität, Würzburg, Germany;
Institut für Immunologie, Universitätsklinikum Schleswig-Holstein Campus Kiel, Kiel, Germany; and
Institut für Zellbiologie, Eberhard-Karls-Universität Tübingen, Tübingen, Germany
Human V
9V
2 T cells recognize phosphorylated nonpeptide Ags (so called phosphoantigens), certain tumor cells, and cells treated with aminobisphosphonates. NKG2D, an activating receptor for NK cells, has been described as a potent costimulatory receptor in the Ag-specific activation of and CD8 T cells. This study provides evidence that V9V2 T cells may also be directly activated by NKG2D. Culture of PBMC with immobilized NKG2D-specific mAb or NKG2D ligand MHC class I related protein A (MICA) induces the up-regulation of CD69 and CD25 in NK and V9V2 but not in CD8 T cells. Furthermore, NKG2D triggers the production of TNF-
but not of IFN-, as well as the release of cytolytic granules by V9V2 T cells. Purified V9V2 T cells kill MICA-transfected RMA mouse cells but not control cells. Finally, DAP10, which mediates NKG2D signaling in human NK cells, was detected in resting and activated V9V2 T cells. These remarkable similarities in NKG2D function in NK and V9V2 T cells may open new perspectives for V9V2 T cell-based immunotherapy, e.g., by Ag-independent killing of NKG2D ligand-expressing tumors.
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