| First Author | Nabekura T | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 5 | Pages | 1567-1571 |
| PubMed ID | 28760883 | Mgi Jnum | J:251619 |
| Mgi Id | MGI:6099426 | Doi | 10.4049/jimmunol.1700799 |
| Citation | Nabekura T, et al. (2017) Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection. J Immunol 199(5):1567-1571 |
| abstractText | 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. |
