Journal
JOURNAL OF IMMUNOLOGY
Volume 199, Issue 5, Pages 1567-1571Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1700799
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Funding
- National Institutes of Health [AI068129, AI066897]
- Parker Institute for Cancer Immunotherapy
- European Research Council Advanced Grant [322693]
- Uehara Memorial Foundation
- Natio Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Japan Society for the Promotion of Science
- Friends of Leukemia Research Fund
- Nakajima Foundation
- Grants-in-Aid for Scientific Research [17H05071, 15J08253] Funding Source: KAKEN
- European Research Council (ERC) [322693] Funding Source: European Research Council (ERC)
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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 2 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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