Altered glucose metabolism in B cells: Implications for the pathogenesis and treatment of autoimmune diseases

Introduction

Metabolic dysregulation in immune cells is increasingly recognized as a contributing factor in autoimmune diseases. B lymphocytes, which play key roles in immune tolerance and autoantibody production, show altered glucose metabolism. This review examines the role of glucose metabolism in B cell function and its potential impact on autoimmune pathogenesis.

Methods

We reviewed evidence from animal and cell-based studies, together with available clinical findings, on glucose metabolic shifts in various B cell subsets—including naïve, activated, germinal center, plasma, and memory B cells—across major autoimmune diseases. Particular attention was given to glycolysis, oxidative phosphorylation (OXPHOS), and mTOR signaling pathways.

Results

Evidence of altered B cell metabolism, especially increased glycolysis, is most extensively documented in systemic lupus erythematosus (SLE), with growing insights emerging in rheumatoid arthritis (RA), Sjögren's syndrome (SS), and type 1 diabetes (T1D). These metabolic changes are associated with B cell activation, autoantibody production, and broader immune modulation. While many findings are based on comparisons with healthy donors, the understanding of disease-specific metabolic patterns is progressively improving.

Conclusion

Altered glucose metabolism appears to be a common, though variable, feature of B cells in autoimmune diseases. Current data suggest distinct metabolic profiles in SLE, RA, SS, and T1D. Although much of the existing evidence is derived from in vitro and animal studies, ongoing research continues to refine our understanding. Further cross-disease comparative investigations—especially in RA, SS, and T1D—will be instrumental in delineating the unique metabolic adaptations underlying each condition.