Obesity is associated with a wide range of complications, including type 2 diabetes mellitus, cardiovascular disease, hypertension and nonalcoholic fatty liver disease. Obesity also increases the incidence and progression of cancers, autoimmunity and infections, as well as lowering vaccine responsiveness. A unifying concept across these differing diseases is dysregulated immunity, particularly inflammation, in response to metabolic overload. Herein, we review emerging mechanisms by which obesity drives inflammation and autoimmunity, as well as impairing tumour immunosurveillance and the response to infections. Among these mechanisms are obesity-associated changes in the hormones that regulate immune cell metabolism and function and drive inflammation. The cargo of extracellular vesicles derived from adipose tissue, which controls cytokine secretion from immune cells, is also dysregulated in obesity, in addition to impairments in fatty acid metabolism related to inflammation. Furthermore, an imbalance exists in obesity in the biosynthesis and levels of polyunsaturated fatty acid-derived oxylipins, which control a range of outcomes related to inflammation, such as immune cell chemotaxis and cytokine production. Finally, there is a need to investigate how obesity influences immunity using innovative model systems that account for the heterogeneous nature of obesity in the human population.

肥胖与多种并发症相关，包括2型糖尿病、心血管疾病、高血压和非酒精性脂肪肝。肥胖还会增加癌症、自身免疫和感染的发病率和进展，并降低疫苗反应性。这些不同疾病的一个统一概念是免疫失调，特别是炎症，以应对代谢超负荷。在此，我们回顾了肥胖引起炎症和自身免疫以及损害肿瘤免疫监视和感染反应的新机制。这些机制包括与肥胖相关的激素变化，这些激素调节免疫细胞的代谢和功能并引发炎症。除了与炎症相关的脂肪酸代谢受损之外，来自脂肪组织的细胞外囊泡的货物控制着免疫细胞的细胞因子分泌，在肥胖症中也会失调。此外，肥胖症中多不饱和脂肪酸衍生的氧脂质的生物合成和水平存在不平衡，氧脂质控制着一系列与炎症相关的结果，例如免疫细胞趋化性和细胞因子的产生。最后，需要使用创新模型系统来研究肥胖如何影响免疫力，该模型系统解释了人群中肥胖的异质性。