Systemic lupus erythematosus (SLE) is a highly heterogeneous autoimmune disease,characterized by production of pathogenic autoantibodies and wide involvement of multiple systems. Damageofimmune tolerance and imbalance of immune homeostasis lead to the production of autoantibodies and the injuries of multiple organs and systems. In recent years,plenty of studies have identified that immunometabolism affects survival status of certain cells,also cell activation,differentiation and effector functions. Conversely,immune cells with different functions or differentiational status upregulate specific me-tabolic pathways to maintain their identities. In response to outer stimulations,naive immune cells dif-ferentiate into activated cells,accompanied with a series of immunometabolism changes. Therefore,abnormal immunometabolism can induce global imbalance of immune homeostasis,which further results in the initiation and development of autoimmune diseases,including SLE. Multiple abnormalities of immunometabolism have been found in patients with SLE or mouse models of lupus. Immune cells involved in the development of SLE,such as T cells,B cells,dendritic cells and macrophages present various metabolic abnormalities and pathological phenotypes. Among these cells,CD4 ⁺ T cells play predominant roles in the pathogenesis of SLE. Lots of studies demonstrated that CD4 ⁺ T cells and their subsets were in abnormal immunometabolic status,which further resulted in the development of SLE. In CD4 ⁺ T cells from patients with SLE or mouse models of lupus,both levels of glycolysis and oxidative phosphorylation are significantly higher compared with healthy controls. However,mitochondrial abnormalities,decreased ATP production and increased level of oxidative stress also have been found in these cells,which play important roles in the production of reactive oxygen intermediates and autoantibodies. Aggregated lipids rafts and increased synthesis of glycosphingolipid and cholesterol also have been observed in the CD4 ⁺ T cells from patients with SLE,leading to the abnormally elevated TCR signaling. Moreover,mechanistic target of rapamycin (mTOR) signaling is activated in the CD4 ⁺ T cells from both patients with SLE or mouse models of lupus and participate in the metabolic abnormalities of pathological CD4 ⁺ T cells. Progressive understanding of immunometabolism give us new insights of the pathogenesis of SLE and provide us with more therapeutic targets in the treatment of SLE.