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The metabolic regulation in immune cells and pathogenesis of systemic lupus erythematosus ∼toward new therapeutic applications∼.


The importance of cellular metabolism has long been known as Warburg effect; cancer cells are characterized by mitochondrial defect that shifts towards aerobic glycolysis. Recently, many reports have revealed that immune metabolism is a key factor for controlling immune cell proliferation and differentiation. Resting lymphocytes generate energy through oxidative phosphorylation and fatty acid oxidation, whereas activated lymphocytes rapidly shift to glycolysis. Especially in T cells, more precise mechanism of regulating metabolism have been clarified on differentiation from naïve T cells to effector T cells. Similar studies have also been carried out to characterize B cell and myeloid cell metabolism. Metabolic regulation is considered to be particularly important in autoimmune diseases. Metabolic changes in these diseases might not only reflect the chronic activated immune-status but also associated with their pathogenesis. Here, we review what is known on the altered metabolism in systemic lupus erythematosus (SLE), mainly focusing on T cells and B cells, and how they contribute to SLE pathogenesis. We also discuss how immune metabolic defects can become targets of future SLE therapy.