| First Author | Nabekura T | Year | 2014 |
| Journal | Immunity | Volume | 40 |
| Issue | 2 | Pages | 225-34 |
| PubMed ID | 24440149 | Mgi Jnum | J:209371 |
| Mgi Id | MGI:5567030 | Doi | 10.1016/j.immuni.2013.12.011 |
| Citation | Nabekura T, et al. (2014) Costimulatory molecule DNAM-1 is essential for optimal differentiation of memory natural killer cells during mouse cytomegalovirus infection. Immunity 40(2):225-34 |
| abstractText | Recent studies demonstrate that natural killer (NK) cells have adaptive immune features. Here, we investigated the role of the costimulatory molecule DNAM-1 in the differentiation of NK cells in a mouse model of cytomegalovirus (MCMV) infection. Antibody blockade of DNAM-1 suppressed the expansion of MCMV-specific Ly49H(+) cells during viral infection and inhibited the generation of memory NK cells. Similarly, DNAM-1-deficient (Cd226(-/-)) Ly49H(+) NK cells exhibited intrinsic defects in expansion and differentiation into memory cells. Src-family tyrosine kinase Fyn and serine-threonine protein kinase C isoform eta (PKCeta) signaling through DNAM-1 played distinct roles in the generation of MCMV-specific effector and memory NK cells. Thus, cooperative signaling through DNAM-1 and Ly49H are required for NK cell-mediated host defense against MCMV infection. |
