The role of B cell glycolysis in autoimmune diseases

Autoimmune diseases are a category of chronic disorders in which the body's immune system fails to distinguish between self-antigens and foreign substances, leading to attacks on its own tissues and subsequent damage. B cells play critical roles in humoral immunity, including antibody production, antigen presentation, and immune regulation. When B cell function is impaired, these cells can contribute to autoimmune diseases by producing autoantibodies and pro-inflammatory cytokines, causing an imbalance in immune regulation. Recent advances in immunometabolism research have revealed that B cell metabolism plays a significant role in immune responses by providing energy and substrates for B cell activation, differentiation, and function. However, dysregulated B cell metabolism disrupts self-tolerance mechanisms, which can trigger autoimmune diseases. This article systematically reviews the manifestations and pathogenic mechanisms of glycolysis dysregulation in B cells in both patients with autoimmune diseases and animal models, and explores the therapeutic potential of targeting glycolysis in autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and type 1 diabetes (T1D). A deeper understanding of the metabolic regulatory mechanisms of B cells will provide an important theoretical foundation for developing novel therapies for autoimmune diseases.