B cell phenotype, activity, and function in idiopathic nephrotic syndrome

Abstract

Idiopathic nephrotic syndrome (INS) is the most frequent glomerular disease in childhood. However, its underlying etiology mechanism lacks thorough understanding. Previous studies have described INS as a T cell functional disorder resulting in increased plasma lymphocyte-derived permeability factors. In children with frequent relapses of nephrotic syndrome, the mechanism underlying the therapeutic efficacy of CD20 monoclonal antibodies in depleting B cells may provide additional evidence in exploring the critical role of B lymphocytes in INS pathogenesis. Previous studies have proposed that RTX bound to CD20 through antibody-dependent and complement-dependent cytotoxicity and led to lytic clearance of B cells. Additionally, RTX exerted an effect by blocking the interaction between B and T cells or regulating homeostasis and functions of T cell subsets. Recent studies on the development, differentiation, and activation of B-lymphocytes in glomerular diseases have suggested that the B-lymphocytes participate in the INS pathogenesis through interaction with T cells, secretion of antibodies, or production of cytokines. In this study, we aimed to provide a detailed description of the current knowledge on the development, differentiation, activity, functions, and related regulating factors of B cells involved in INS. Thus, further understanding of the immunopathogenesis of INS may offer some opportunities in precisely targeting B cells during therapeutic interventions. IMPACT: The topic "B cells play a role in glomerular disease" is a novel point, which is not completely described previously. We described interactions between T and B cells and immunoglobulin, IgG, IgM, IgE, etc. as well in glomerular disease. The research of regulatory factors associated with B cell's function, like BAFF, is a hot topic in other diseases; however, it is rare in glomerular disease.