| First Author | Wilk S | Year | 2013 |
| Journal | Eur J Immunol | Volume | 43 |
| Issue | 4 | Pages | 1024-33 |
| PubMed ID | 23401034 | Mgi Jnum | J:195047 |
| Mgi Id | MGI:5476367 | Doi | 10.1002/eji.201242382 |
| Citation | Wilk S, et al. (2013) Adiponectin modulates NK-cell function. Eur J Immunol 43(4):1024-33 |
| abstractText | Adiponectin (APN) has been shown to exert antiinflammatory effects in various disease models but little is known concerning its regulation of NK-cell function. Here, we show that the majority of human CD56(dim) NK cells express surface Adiponectin receptor (AdipoR) 1 and 2 while most CD56(high) NK cells are AdipoR-negative. Toll-like receptor (TLR) ligand-induced IFN-gamma production was diminished by APN while it had no influence on NK-cell cytotoxicity. In contrast only a small subpopulation of murine NK cells expresses surface AdipoRs, but about 90% store them intracellularly. APN-deficient knockout (KO) mice had elevated frequencies of NK cells. However, cytotoxic degranulation of NK cells was decreased in APN knockout (APN-KO) animals. Accordingly, frequencies of CD11b(high) CD27(high) and CD94(high) effector NK cells and expression of NKG2D were lower in APN-KO mice. Upon CVB3 infection NK-cell function was restored in APN-KO mice. Our data suggest that in addition to its antiinflammatory effects APN also influences the numerical and differentiation status of NK cells, which may further impact the outcome of immune-mediated diseases in APN-KO mice. |
