Autoimmune diseases (AIDs) are characterized with aberrant immune responses and their respective signaling pathways controlling cell differentiation, death, and survival. Cell metabolism is also an indispensable biochemical process that provides the very fundamental energy and materials. Accumulating evidences implicate that metabolism pathways have critical roles in determining the function of different immune subsets. Mechanisms of how immunometabolism participate in the pathogenesis of AIDs were also under intensive exploration. Here, in this review, we summarize the metabolic features of immune cells in AIDs and also the individual function of immunometabolism pathways, including glucose metabolism and tricarboxylic acid (TCA) cycle, in the setting of AIDs, mainly focusing on the potential targets for intervention. We also review studies that explore the intervention strategies targeting key molecules of metabolic pathways, such as mammalian target of rapamycin (mTOR), AMP-activated protein kinase (AMPK), and hypoxia-inducible factor 1a (HIF1a), in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The highlight of this review is to provide a comprehensive summary of the status quo of immunometabolism studies in AIDs and the potential translatable drug targets.

自身免疫性疾病 (AID) 的特征是异常的免疫反应及其各自控制细胞分化、死亡和存活的信号通路。细胞代谢也是一个不可或缺的生化过程，提供非常基本的能量和材料。越来越多的证据表明，代谢途径在确定不同免疫亚群的功能方面具有关键作用。免疫代谢如何参与艾滋病发病机制的机制也在深入探索中。在这里，在这篇综述中，我们总结了 AIDs 中免疫细胞的代谢特征以及免疫代谢途径的个体功能，包括在 AIDs 的设置中，包括葡萄糖代谢和三羧酸 (TCA) 循环，主要关注干预的潜在目标. 我们还回顾了探索针对系统性红斑狼疮中代谢途径关键分子的干预策略的研究，例如哺乳动物雷帕霉素靶蛋白 (mTOR)、AMP 活化蛋白激酶 (AMPK) 和缺氧诱导因子 1a (HIF1a)。 SLE) 和类风湿性关节炎 (RA)。本综述的重点是对艾滋病免疫代谢研究的现状和潜在的可转化药物靶点进行全面总结。.