Abstract

Obesity is characterized by low-grade, chronic inflammation, which promotes insulin resistance and diabetes. Obesity can lead to the development and progression of many autoimmune diseases, including inflammatory bowel disease, psoriasis, psoriatic arthritis, rheumatoid arthritis, thyroid autoimmunity, and type 1 diabetes mellitus (T1DM). These diseases result from an alteration of self-tolerance by promoting pro-inflammatory immune response by lowering numbers of regulatory T cells (T_regs), increasing Th1 and Th17 immune responses, and inflammatory cytokine production. Therefore, understanding the immunological changes that lead to this low-grade inflammatory milieu becomes crucial for the development of therapies that suppress the risk of autoimmune diseases and other immunological conditions. Cells generate extracellular vesicles (EVs) to eliminate cellular waste as well as communicating the adjacent and distant cells through exchanging the components (genetic material [DNA or RNA], lipids, and proteins) between them. Immune cells and adipocytes from individuals with obesity and a high basal metabolic index (BMI) produce also release exosomes (EXOs) and microvesicles (MVs), which are collectively called EVs. These EVs play a crucial role in the development of autoimmune diseases. The current review discusses the immunological dysregulation that leads to inflammation, inflammatory diseases associated with obesity, and the role played by EXOs and MVs in the induction and progression of this devastating conditi8on.

摘要

肥胖的特征是低度、慢性炎症，这会促进胰岛素抵抗和糖尿病。肥胖会导致许多自身免疫性疾病的发生和发展，包括炎症性肠病、银屑病、银屑病关节炎、类风湿性关节炎、甲状腺自身免疫病和 1 型糖尿病 (T1DM)。这些疾病是由于通过降低调节性 T 细胞 ( T _{regs ) 的数量来促进促炎免疫反应而改变自身耐受性})，增加 Th1 和 Th17 免疫反应，以及炎性细胞因子的产生。因此，了解导致这种低度炎症环境的免疫变化对于开发抑制自身免疫性疾病和其他免疫疾病风险的疗法至关重要。细胞产生细胞外囊泡 (EV) 以消除细胞废物，并通过交换它们之间的成分（遗传物质 [DNA 或 RNA]、脂质和蛋白质）来与相邻和远处的细胞进行通信。来自肥胖和高基础代谢指数 (BMI) 个体的免疫细胞和脂肪细胞也会释放外泌体 (EXO) 和微泡 (MV)，它们统称为 EV。这些 EV 在自身免疫性疾病的发展中起着至关重要的作用。