Article: article from journal or magazin.
Type I interferons protect T cells against NK cell attack mediated by the activating receptor NCR1.
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
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.
Adoptive Transfer, Animals, Antigens, Ly/immunology, CD4-Positive T-Lymphocytes/immunology, CD8-Positive T-Lymphocytes/immunology, Cells, Cultured, Cytotoxicity, Immunologic, Immunity, Innate, Interferon Type I/immunology, Killer Cells, Natural/immunology, Lymphocyte Activation/immunology, Lymphocytic Choriomeningitis/immunology, Lymphocytic Choriomeningitis/virology, Lymphocytic choriomeningitis virus/immunology, Mice, Mice, Inbred C57BL, Mice, Knockout, Natural Cytotoxicity Triggering Receptor 1/immunology, Perforin/biosynthesis, Receptor, Interferon alpha-beta/genetics, Rhabdoviridae Infections/immunology, Signal Transduction/immunology, Vesiculovirus/genetics, Vesiculovirus/immunology, Virus Replication/immunology
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