B-Cell Modulators in IgA Nephropathy: An Interview

Posted on July 29, 2026 by AJKDblog in Interview, Video // 0 Comments

In IgA nephropathy (IgAN), elevated levels of the circulating autoantigen galactose-deficient IgA1 are critical to disease pathogenesis. Genetic as well as in vitro, in vivo, and human immunologic studies have identified APRIL (a proliferation-inducing ligand) and BAFF (B-cell activating factor) as key cytokines controlling B-cell development and the differentiation of antibody-secreting cells. A recent Mini Review published in AJKD by Reily et al covers key aspects related to the roles of APRIL and BAFF in the pathogenesis of IgAN and the significance of their therapeutic targeting.

IgA B cell migration and mucosal immune system. B-cell differentiation and maturation into IgA1-secreting cells starts with early development from progenitor B cells in the bone marrow into naive B cells, migrating to inductive sites across the body. Secondary lymph organs, such as spleen, mesenteric lymph nodes in the gut (such as Peyer’s patches in the upper and lower intestines), tonsils, and bronchus-associated lymph serve as inductive sites where naive B cells enter the germinal centers for further development. Here T-cell-dependent and independent signaling drives class-switch recombination of IgM+ or IgD+ naive B cells into IgA+, IgG+, or IgE+ cells. These cells can be in the form of plasmablasts, B-cell memory, plasma or antibody-secreting cells, or long-lived plasma cells. IgA+ class-switched B cells migrate from the germinal centers to effector sites based on their cell surface homing receptors. Created with BioRender.com. Abbreviations: ASC, antibody-secreting cell; PB, plasmablasts. Figure 2 from Reily et al, © National Kidney Foundation.

AJKDBlog’sInterviews Editor Timothy Yau chatted with author Dana Rizk about the tremendous advancements over the last few years in the understanding of IgAN pathogenesis in which B cells and their products play a central role.