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Immunity. 2014 Jun 19;40(6):961-73. doi: 10.1016/j.immuni.2014.05.003. Epub 2014 Jun 5.

Type I interferons protect T cells against NK cell attack mediated by the activating receptor NCR1.

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Institute of Microbiology, ETH Zürich, 8093 Zurich, Switzerland.
Vital-IT, Swiss Institute of Bioinformatics, CHUV, University of Lausanne, 1015 Lausanne, Switzerland.
Innsbruck Medical University, 6020 Innsbruck, Austria.
Institute for Experimental Infection Research, TWINCORE, Center for Experimental and Clinical Infection Research, Helmholtz Centre for Infection Research, Braunschweig, and Hannover Medical School, 30625 Hannover, Germany.
Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale, U1104, Marseille, France.
Department of Histology and Embryology, Faculty of Medicine, 51000 Rijeka, Croatia.
Institute of Microbiology, ETH Zürich, 8093 Zurich, Switzerland. Electronic address:


Direct type I interferon (IFN) signaling on T cells is necessary for the proper expansion, differentiation, and survival of responding T cells following infection with viruses prominently inducing type I IFN. The reasons for the abortive response of T cells lacking the type I IFN receptor (Ifnar1(-/-)) remain unclear. We report here that Ifnar1(-/-) T cells were highly susceptible to natural killer (NK) cell-mediated killing in a perforin-dependent manner. Depletion of NK cells prior to lymphocytic choriomeningitis virus (LCMV) infection completely restored the early expansion of Ifnar1(-/-) T cells. Ifnar1(-/-) T cells had elevated expression of natural cytotoxicity triggering receptor 1 (NCR1) ligands upon infection, rendering them targets for NCR1 mediated NK cell attack. Thus, direct sensing of type I IFNs by T cells protects them from NK cell killing by regulating the expression of NCR1 ligands, thereby revealing a mechanism by which T cells can evade the potent cytotoxic activity of NK cells.

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