McLaughlin Tracey, Ackerman Shelley E, Shen Lei, Engleman Edgar
J Clin Invest. 2017 Jan 3;127(1):5-13. doi: 10.1172/JCI88876.
Chronic inflammation in adipose tissue, possibly related to adipose cell hypertrophy, hypoxia, and/or intestinal leakage of bacteria and their metabolic products, likely plays a critical role in the development of obesity-associated insulin resistance (IR). Cells of both the innate and adaptive immune system residing in adipose tissues, as well as in the intestine, participate in this process. Thus, M1 macrophages, IFN-γ-secreting Th1 cells, CD8+ T cells, and B cells promote IR, in part through secretion of proinflammatory cytokines. Conversely, eosinophils, Th2 T cells, type 2 innate lymphoid cells, and possibly Foxp3+ Tregs protect against IR through local control of inflammation.
脂肪组织中的慢性炎症可能与脂肪细胞肥大、缺氧和/或细菌及其代谢产物的肠道渗漏有关,它可能在肥胖相关胰岛素抵抗(IR)的发展中起关键作用。驻留在脂肪组织以及肠道中的先天性和适应性免疫系统的细胞都参与了这一过程。因此,M1巨噬细胞、分泌IFN-γ的Th1细胞、CD8+T细胞和B细胞部分通过分泌促炎细胞因子来促进胰岛素抵抗。相反,嗜酸性粒细胞、Th2 T细胞、2型先天性淋巴细胞以及可能的Foxp3+调节性T细胞通过局部控制炎症来预防胰岛素抵抗。