Adiponectin modulates NK-cell function

Eur J Immunol. 2013 Apr;43(4):1024-33. doi: 10.1002/eji.201242382. Epub 2013 Mar 1.


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-γ 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / genetics
  • Adiponectin / metabolism*
  • Animals
  • Cell Degranulation / immunology
  • Cells, Cultured
  • Cytotoxicity, Immunologic
  • Gene Expression Regulation
  • Humans
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / genetics
  • Killer Cells, Natural / immunology*
  • Killer Cells, Natural / metabolism*
  • Ligands
  • Mice
  • Mice, Knockout
  • Receptors, Adiponectin / genetics
  • Receptors, Adiponectin / metabolism
  • Toll-Like Receptors / metabolism


  • Adiponectin
  • Ligands
  • Receptors, Adiponectin
  • Toll-Like Receptors
  • Interferon-gamma