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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.

Author information

1
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143.
2
Parker Institute for Cancer Immunotherapy, San Francisco, CA 94143.
3
Life Science Center, Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki 305-8577, Japan.
4
Ph.D. Program in Human Biology, School of Integrative and Global Majors, University of Tsukuba, Ibaraki 305-8575, Japan; and.
5
Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka 51000, Croatia.
6
Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143; Lewis.Lanier@ucsf.edu.

Abstract

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.

PMID:
28760883
PMCID:
PMC5567695
DOI:
10.4049/jimmunol.1700799
[Indexed for MEDLINE]
Free PMC Article

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