期刊
NATURE IMMUNOLOGY
卷 15, 期 5, 页码 423-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2865
关键词
-
类别
资金
- Deutsche Forschungsgemeinschaft [SFB 612, SFB 670]
- Leibniz Preis [BR 1492/7-1]
- US National Institutes of Health [DP1AR064158, HL076746, DK094641]
- National Health and Medical Research Council of Australia [APP1041760, APP1042465, SPRF APP1021168]
Obesity and resistance to insulin are closely associated with the development of low-grade inflammation. Interleukin 6 (IL-6) is linked to obesity-associated inflammation; however, its role in this context remains controversial. Here we found that mice with an inactivated gene encoding the IL-6R. chain of the receptor for IL-6 in myeloid cells (116ra(Delta myel) mice) developed exaggerated deterioration of glucose homeostasis during diet-induced obesity, due to enhanced resistance to insulin. Tissues targeted by insulin showed increased inflammation and a shift in macrophage polarization. IL-6 induced expression of the receptor for IL-4 and augmented the response to IL-4 in macrophages in a cell-autonomous manner. 116ra(Delta myel) mice were resistant to IL-4-mediated alternative polarization of macrophages and exhibited enhanced susceptibility to lipopolysaccharide (LPS)-induced endotoxemia. Our results identify signaling via IL-6 as an important determinant of the alternative activation of macrophages and assign an unexpected homeostatic role to IL-6 in limiting inflammation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据