Immune regulation and cell metabolism in B cell subsets in patients with systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is an autoimmune disease that predominantly affects young women and involves multiple organs, including the skin, joints, kidneys, and nervous system. In the pathogenesis of SLE, autoreactive B cells play a pivotal role through mediating antibody production, antigen presentation, and cytokine secretion. Recent studies have highlighted immunometabolism as a pivotal regulatory axis operating at both intracellular and extracellular levels during immune dysregulation. In SLE, plasma cells produce large quantities of autoantibodies, playing an important role in disease progression. This process demands a substantial energy supply, along with protein and nucleic acid synthesis, and is accompanied by dynamic reconstitution of intracellular metabolism. Furthermore, alterations in metabolic pathways not only facilitate efficient energy production but also directly modulate immune responses, including cytokine production and cell differentiation. Differences in cellular metabolism can shape B cell differentiation trajectories. Elucidating the immunometabolic mechanisms governing B cell activation and fate decisions may reveal novel drivers of lupus pathogenesis and identify new opportunities for therapeutic intervention.