Autoimmune diseases are common diseases of the immune system that are characterized by the loss of self-tolerance and the production of autoantibodies; the breakdown of immune tolerance and the prolonged inflammatory reaction are undisputedly core steps in the initiation and maintenance of autoimmunity. Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors that belong to the nuclear hormone receptor family and act as ligand-activated transcription factors. There are three different isotypes of PPARs: PPARα, PPARγ, and PPARβ/δ. PPARγ is an established regulator of glucose homeostasis and lipid metabolism. Recent studies have demonstrated that PPARγ exhibits anti-inflammatory and anti-fibrotic effects in multiple disease models. PPARγ can also modulate the activation and polarization of macrophages, regulate the function of dendritic cells and mediate T cell survival, activation, and differentiation. In this review, we summarize the signaling pathways and biological functions of PPARγ and focus on how PPARγ and its agonists play protective roles in autoimmune diseases, including autoimmune thyroid diseases, multiple sclerosis, rheumatoid arthritis, systemic sclerosis, systemic lupus erythematosus, primary Sjogren syndrome and primary biliary cirrhosis.

自身免疫性疾病是免疫系统的常见疾病，其特征是自身耐受性丧失和自身抗体的产生；免疫耐受性的崩溃和长时间的炎症反应无疑是自身免疫启动和维持的核心步骤。过氧化物酶体增殖物激活受体 (PPAR) 是配体依赖性转录因子，属于核激素受体家族，充当配体激活转录因子。存在三种不同的 PPAR 同种型：PPARα、PPARγ 和 PPARβ/δ。PPARγ 是葡萄糖稳态和脂质代谢的既定调节剂。最近的研究表明，PPARγ 在多种疾病模型中表现出抗炎和抗纤维化作用。PPARγ 还可以调节巨噬细胞的活化和极化，调节树突状细胞的功能并介导 T 细胞的存活、激活和分化。在这篇综述中，我们总结了PPARγ的信号通路和生物学功能，并重点介绍了PPARγ及其激动剂如何在自身免疫性疾病中发挥保护作用，包括自身免疫性甲状腺疾病、多发性硬化症、类风湿性关节炎、系统性硬化症、系统性红斑狼疮、原发性干燥综合征和原发性胆汁性肝硬化。