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

机译：IL-6 / STAT3依赖性诱导明显，肥胖相关的NK细胞亚群劣化能量和葡萄糖稳态

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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.
机译：天然杀手（NK）细胞有助于肥胖相关的胰岛素抵抗的发展。我们证明，在小鼠肥胖症中，促进了不同白细胞介素-6受体（IL6R）A表达的NK亚群的扩增，其还表达了许多其他髓样谱系，例如菌落刺激因子1受体（CSF1R）。选择性消融该CSF1R表达的NK细胞群可防止肥胖和胰岛素抵抗力。此外，NK细胞IL6RA或STAT3的条件失活限制了这些髓样特征NK细胞的肥胖相关的形成，保护免受肥胖，胰岛素抵抗和肥胖症相关的炎症。同样在人体IL6RA（+）NK细胞中肥胖的增加和与系统性低级炎症的标志物相关，它们的基因表达谱与肥胖小鼠中的NK细胞的特征基因组重叠。统称，我们证明肥胖相关的炎症和代谢紊乱取决于表现素-6 / STAT3依赖性形成不同的NK群体，这可以为治疗肥胖，均法相关病理和糖尿病提供靶标。

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