Journal
CELL METABOLISM
Volume 26, Issue 1, Pages 171-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2017.05.018
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Funding
- Medical Faculty, University of Cologne, Germany [3/2014]
- Deutsche Forschungsgemeinschaft (DFG) [BR 1492/7-1, TRR134, SFB829]
- Excellence Initiative of the German Federal and State Governments (CECAD)
- ICEMED (Imaging and Curing Environmental Metabolic Diseases) Initiative
- Networking Fund of the Helmholtz Association
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Natural killer (NK) cells contribute to the development of obesity-associated insulin resistance. We demonstrate that in mice obesity promotes expansion of a distinct, interleukin-6 receptor (IL6R) a-expressing NK subpopulation, which also expresses a number of other myeloid lineage genes such as the colony-stimulating factor 1 receptor (Csf1r). Selective ablation of this Csf1r-expressing NK cell population prevents obesity and insulin resistance. Moreover, conditional inactivation of IL6Ra or Stat3 in NK cells limits obesity-associated formation of these myeloid signature NK cells, protecting from obesity, insulin resistance, and obesity-associated inflammation. Also in humans IL6Ra(+) NK cells increase in obesity and correlate with markers of systemic low-grade inflammation, and their gene expression profile overlaps with characteristic gene sets of NK cells in obese mice. Collectively, we demonstrate that obesity-associated inflammation and metabolic disturbances depend on interleukin-6/Stat3-dependent formation of a distinct NK population, which may provide a target for the treatment of obesity, metaflammation-associated pathologies, and diabetes.
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