Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by excessive autoantibody production and multi-organ involvement. Although the etiology of SLE still remains unclear, recent studies have characterized several pathogenic B cell subsets and regulatory B cell subsets involved in the pathogenesis of SLE. Among pathogenic B cell subsets, age-associated B cells (ABCs) are a newly identified subset of autoreactive B cells with T-bet-dependent transcriptional programs and unique functional features in SLE. Accumulation of T-bet+ CD11c+ ABCs has been observed in SLE patients and lupus mouse models. In addition, innate-like B cells with the autoreactive B cell receptor (BCR) expression and long-lived plasma cells with persistent autoantibody production contribute to the development of SLE. Moreover, several regulatory B cell subsets with immune suppressive functions have been identified, while the impaired inhibitory effects of regulatory B cells have been indicated in SLE. Thus, further elucidation on the functional features of B cell subsets will provide new insights in understanding lupus pathogenesis and lead to novel therapeutic interventions in the treatment of SLE.
Highlights
The immune system recognizes pathogens from the external environment and initiates protective immune responses, but ignores antigens derived from the host to maintain immune tolerance [1]
The expanded CD11b+CD11c+ B cells in peripheral blood mononuclear cells (PBMCs) of Systemic lupus erythematosus (SLE) patients observed in early studies appeared to be B-1 cells, which was further supported by more recent findings that the frequencies of B-1 cells were markedly increased in SLE patients [32]
marginal zone (MZ) B cells contribute to the progression of lupus in mice, both phenotypic features and functional properties of MZ B cells need to be further investigated in humans
Summary
The immune system recognizes pathogens from the external environment and initiates protective immune responses, but ignores antigens derived from the host to maintain immune tolerance [1]. Systemic lupus erythematosus (SLE) is a severe autoimmune disease, in which anti-nuclear antibodies (ANAs) and autoreactive B cells play crucial roles during disease progression and target organ damages [3,4,5,6]. In addition to autoantibody secretion, B cells perform multiple functions in the immune system, including antigen presentation and cytokine secretion [18]. SLE patients with multiple courses of rituximab treatment even developed rituximab resistance, indicating the complexity of abnormal B cell-mediated immunity [21,22]. Current studies have suggested that both impairments of Breg cell functions and expansions of autoreactive B subsets lead to immune tolerance breakdown and autoimmune progression [27].
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