IL-6/Stat3-Dependent Induction of a Distinct, Obesity-Associated NK Cell 
Subpopulation Deteriorates Energy and Glucose Homeostasis

Theurich, S.; Tsaousidou, E.; Hanssen, R.; Lempradl, A. M.; Mauer, J.; Timper, K.; Schilbach, K.; Folz-Donahue, K.; Heilinger, C.; Sexl, V.; Pospisilik, J. A.; Wunderlich, F. T.; Bruning, J. C.

doi:10.1016/j.cmet.2017.05.018

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IL-6/Stat3-Dependent Induction of a Distinct, Obesity-Associated NK Cell Subpopulation Deteriorates Energy and Glucose Homeostasis

MPS-Authors

Theurich, S.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Tsaousidou, E.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Hanssen, R.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Lempradl, A. M.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Mauer, J.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Timper, K.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Schilbach, K.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Folz-Donahue, K.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Heilinger, C.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Sexl, V.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Pospisilik, J. A.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Wunderlich, F. T.
Max Planck Institute for Biology of Ageing, Max Planck Society;

Bruning, J. C.
Max Planck Institute for Biology of Ageing, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/28683285
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Citation

Theurich, S., Tsaousidou, E., Hanssen, R., Lempradl, A. M., Mauer, J., Timper, K., et al. (2017). IL-6/Stat3-Dependent Induction of a Distinct, Obesity-Associated NK Cell Subpopulation Deteriorates Energy and Glucose Homeostasis. Cell Metab, 26(1), 171-184 e6. doi:10.1016/j.cmet.2017.05.018.

Cite as: https://hdl.handle.net/21.11116/0000-0001-5938-D

Abstract

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.