Paul-Langerhans Group, German Diabetes Center, Leibniz Center for Diabetes Research at the Heinrich-Heine-University Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Nat Rev Endocrinol. 2012 Dec;8(12):709-16. doi: 10.1038/nrendo.2012.114. Epub 2012 Jul 31.
Obesity is the hallmark of the metabolic syndrome and predisposes patients to the development of major chronic metabolic diseases including type 2 diabetes mellitus. Adipose tissue expansion in obesity is characterized by increasing infiltration of proinflammatory immune cells into adipose tissue causing chronic, low-grade inflammation. Phenotypic switching of macrophages is an important mechanism of adipose tissue inflammation, and there is involvement of cells from the adaptive immune system in this process. T-cell phenotype changes and recruitment of B cells and T cells precedes macrophage infiltration. Cytokines and chemokines produced by immune cells influence localized and systemic inflammation, which is a pathogenic link between obesity and insulin resistance. Antigens absorbed from the gut might contribute to T-cell activation and recruitment into visceral adipose tissue in obesity. This Review summarizes, in the context of obesity, the evidence for infiltration of adipose tissue by cells of the adaptive immune system, how adaptive system cells affect innate cell populations and the influence of adaptive immune cells on the development of insulin resistance.
肥胖是代谢综合征的标志，并使患者易患包括 2 型糖尿病在内的主要慢性代谢疾病。肥胖症中脂肪组织的扩张表现为促炎免疫细胞浸润到脂肪组织中，导致慢性、低度炎症。巨噬细胞表型转换是脂肪组织炎症的一个重要机制，适应性免疫系统细胞也参与了这个过程。T 细胞表型变化以及 B 细胞和 T 细胞的募集先于巨噬细胞浸润。免疫细胞产生的细胞因子和趋化因子影响局部和全身炎症，这是肥胖和胰岛素抵抗之间的一个致病联系。从肠道吸收的抗原可能有助于 T 细胞在肥胖症中的活化和募集到内脏脂肪组织。本综述在肥胖的背景下总结了适应性免疫系统细胞浸润脂肪组织的证据、适应性系统细胞如何影响先天细胞群体以及适应性免疫细胞对胰岛素抵抗发展的影响。
