Medicine

Xinfeng Wu, Xin Ma, Bei Zhang, Na Kang, Yian Liu, Xiaofei Shi, Wanli Liu

2026.1.30MOLECULAR IMMUNOLOGY

DOI: 10.1016/j.molimm.2026.01.009

tlooto Summary

This review examines the mechanisms linking aberrant B cell activation to SLE development, highlights recent genetic, epigenetic, and clinical insights, and discusses their implications for therapeutic management, providing a useful resource for researchers and clinicians in immunology and autoimmunity.

Abstract

B cells are pivotal components of the immune system, responsible for antibody production and immune regulation. Aberrant B cell activation is central to the pathogenesis of systemic lupus erythematosus (SLE), driven by dysregulations of multiply signaling pathways, including B cell receptor (BCR), Toll-like receptor (TLR7/9), B cell-activating factor receptor (BAFF-R), and B-T cell interactions, along with related cytokines and interferons. These aberrant signaling pathways play diverse and integrated roles in SLE progression, contributing to autoantibody generation and tissue damage. This review examines the mechanisms linking aberrant B cell activation to SLE development, highlights recent genetic, epigenetic, and clinical insights, and discusses their implications for therapeutic management. Collectively, it provides a useful resource for researchers and clinicians in immunology and autoimmunity, enhancing the comprehension of B cell dysregulation in SLE.

Citation format

WU, Xinfeng, et al. The dysregulation of b cells in systemic lupus erythematosus. MOLECULAR IMMUNOLOGY, 2026, 190: 152–161.