Department of Immunology, Yamagata University Faculty of Medicine, Yamagata 990-9585, Japan.
Research Center for Molecular Genetics, Institute for Promotion of Medical Science Research, Yamagata University Faculty of Medicine, Yamagata 990-9585, Japan.
Int J Mol Sci. 2021 Sep 16;22(18):10017. doi: 10.3390/ijms221810017.
Metabolic syndrome results from multiple risk factors that arise from insulin resistance induced by abnormal fat deposition. Chronic inflammation owing to obesity primarily results from the recruitment of pro-inflammatory M1 macrophages into the adipose tissue stroma, as the adipocytes within become hypertrophied. During obesity-induced inflammation in adipose tissue, pro-inflammatory cytokines are produced by macrophages and recruit further pro-inflammatory immune cells into the adipose tissue to boost the immune response. Here, we provide an overview of the biology of macrophages in adipose tissue and the relationship between other immune cells, such as CD4+ T cells, natural killer cells, and innate lymphoid cells, and obesity and type 2 diabetes. Finally, we discuss the link between the human pathology and immune response and metabolism and further highlight potential therapeutic targets for the treatment of metabolic disorders.
代谢综合征是由胰岛素抵抗引起的多种异常脂肪沉积的风险因素所致。肥胖引起的慢性炎症主要是由于促炎 M1 巨噬细胞募集到脂肪组织基质中，导致脂肪细胞肥大。在肥胖引起的脂肪组织炎症中，巨噬细胞产生促炎细胞因子，并募集更多的促炎免疫细胞进入脂肪组织，以增强免疫反应。在这里，我们概述了脂肪组织中巨噬细胞的生物学特性，以及其他免疫细胞（如 CD4+T 细胞、自然杀伤细胞和先天淋巴细胞）与肥胖和 2 型糖尿病之间的关系。最后，我们讨论了人类病理学与免疫反应、代谢之间的联系，并进一步强调了治疗代谢紊乱的潜在治疗靶点。
