The role of double-negative B cells in the pathogenesis of systemic lupus erythematosus

Abstract

B cells are essential to the pathophysiology of systemic lupus erythematosus (SLE), a chronic autoimmune illness. IgD-CD27-double negative B cells (DNB cells) are one of the aberrant B cell subsets linked to SLE that have attracted much scientific interest. There is growing evidence that DNB cells play a significant role in the development of the disease and are strongly linked to the activity of lupus. These cells play a pivotal role in the pathogenesis of SLE by producing a diverse array of autoantibodies, which form immune complexes that drive target organ damage. A comprehensive understanding of SLE pathophysiology necessitates in-depth investigation into DNB cells, not only to elucidate their mechanistic contributions but also to uncover novel therapeutic strategies.

According to available data, treatments that target B cells have proven effective in managing SLE; nevertheless, a significant breakthrough in precision medicine for SLE may come from targeting DNB cells specifically. Despite growing interest in DNB cells, their precise characteristics, developmental trajectories, and regulatory mechanisms remain incompletely defined, posing significant challenges to the field. A comprehensive investigation of the regulatory mechanisms governing DNB cell differentiation and expansion in SLE may facilitate novel therapeutic discoveries. This review aims to provide an updated synthesis of current research on DNB cells, with a focus on their origins, developmental trajectories in SLE, and potential as precision therapeutic targets.