Autoimmune diseases occur when the immune system malfunctions, failing to recognize the body's own tissues or organs and subsequently attacking healthy cells [1,2]. In recent years, the incidence of autoimmune diseases has increased significantly [3], with annual growth rates of 19.1 % for incidence and 12.5 % for prevalence [4]. Common autoimmune diseases include SLE, RA, and SS. Their pathogenesis is complex, involving intricate interactions among genetic, environmental, and immune factors [5]. Given the heterogeneity and complexity of autoimmune diseases, effective treatment remains a major challenge in medicine. Chronic inflammation not only severely impairs patients' quality of life but can also lead to organ damage and life-threatening complications. Current therapeutic approaches primarily involve immunosuppressants and glucocorticoids. However, long-term use may cause serious adverse effects, including diabetes, osteoporosis, myopathy, osteonecrosis and Cushing's syndrome. Beyond impairing quality of life, such complications may culminate in life-threatening consequences in advanced stages [6,7].

Under physiological conditions, B cells orchestrate adaptive immunity through antigen-specific activation, subsequently differentiating into antibody-secreting plasma cells that neutralize exogenous pathogens. In autoimmune pathogenesis, antigen-experienced B cells differentiate into plasma cells that secrete pathogenic autoantibodies. These immunoglobulins contribute to tissue damage in RA, SLE, and T1D by engaging Fcγ receptors, triggering mechanisms such as complement activation and antibody-dependent cellular cytotoxicity (ADCC) [8,9]. In SLE, anti-nuclear antibodies (ANAs) secreted by B cell-derived plasma cells bind to nuclear components of autologous cells, triggering multi-organ damage via immune complex-mediated inflammation [10,11]. B cells also act as antigen-presenting cells by delivering self-antigens to T cells, which leads to T cell activation and promotes the secretion of pro-inflammatory cytokines, intensifying the autoimmune reaction [12,13]. Although most existing original data focus on SLE, a few emerging studies have explored B cell metabolic reprogramming in RA, SS, and T1D. While these findings are still preliminary, they suggest that metabolic alterations in B cells may also be relevant in other autoimmune diseases and warrant further investigation.