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J Immunol. 2017 Sep 1;199(5):1567-1571. doi: 10.4049/jimmunol.1700799. Epub 2017 Jul 31.

Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection.

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Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143.
Parker Institute for Cancer Immunotherapy, San Francisco, CA 94143.
Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki 305-8577, Japan.
Ph.D. Program in Human Biology, School of Integrative and Global Majors, University of Tsukuba, Ibaraki 305-8575, Japan; and.
Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka 51000, Croatia.
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143;


NK cells play a critical role in host defense against viruses. In this study, we investigated the role of NKG2D in the expansion of NK cells after mouse CMV (MCMV) infection. Wild-type and NKG2D-deficient (Klrk1-/- ) Ly49H+ NK cells proliferated robustly when infected with MCMV strains engineered to allow expression of NKG2D ligands, which enhanced the response of wild-type NK cells. Naive NK cells exclusively express NKG2D-L, which pairs only with DAP10, whereas NKG2D-S expressed by activated NK cells pairs with DAP10 and DAP12, similar to Ly49H. However, NKG2D alone was unable to drive robust expansion of Ly49H- NK cells when mice were infected with these MCMV strains, likely because NKG2D-S was only transiently expressed postinfection. These findings demonstrate that NKG2D augments Ly49H-dependent proliferation of NK cells; however, NKG2D signaling alone is inadequate for expansion of NK cells, likely due to only transient expression of the NKG2D-DAP12 complex.

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