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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.

Author information

1
Institute of Microbiology, ETH Zürich, 8093 Zurich, Switzerland.
2
Vital-IT, Swiss Institute of Bioinformatics, CHUV, University of Lausanne, 1015 Lausanne, Switzerland.
3
Innsbruck Medical University, 6020 Innsbruck, Austria.
4
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.
5
Centre d'Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale, U1104, Marseille, France.
6
Department of Histology and Embryology, Faculty of Medicine, 51000 Rijeka, Croatia.
7
Institute of Microbiology, ETH Zürich, 8093 Zurich, Switzerland. Electronic address: oxenius@micro.biol.ethz.ch.

Abstract

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.

PMID:
24909889
DOI:
10.1016/j.immuni.2014.05.003
[Indexed for MEDLINE]
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