Fig. 6

Energy metabolism in autoimmune diseases. In autoimmune diseases, metabolic abnormalities in immune cells are a key factor. In some situations, CD4⁺ T cells enhance glycolysis and mitochondrial OXPHOS, while in rheumatoid arthritis (RA), T cells suffer from impaired mitochondrial OXPHOS, turning to the pentose phosphate pathway. Naive Th cells and B cells tend to undergo aerobic oxidation, while activated Th cells and B cells tend to undergo glycolysis. Treg cells can utilize glycolysis and lactate to maintain their functions in the TME. M1 macrophages tend to have aerobic glycolysis, while M2 macrophages rely more on OXPHOS. FLSs undergo metabolic reprogramming, shifting towards enhanced glycolysis. As antigen-presenting cells, DCs significantly alter their metabolic pathways, such as OXPHOS and glycolysis, during activation. These changes in energy metabolism promote the abnormal proliferation of fibers and blood vessels and exacerbate the inflammatory process. DC dendritic cells, FLS fibroblast-like synoviocytes, Treg regulatory T cells, MDSC myeloid-derived suppressor cells