New insights into the mucosal immune pathogenesis of IgA nephropathy from the perspective of COVID-19 vaccination

Abstract

Large-scale SARS-CoV-2 vaccination is one of the key strategies to curb the COVID-19 pandemic; however, there are increasing reports of IgA nephropathy following COVID-19 vaccination. The clinical manifestation, treatment and prognostic effects are different in IgAN patients who have had an onset after the first and second dose of vaccination, as well as new and recurrent IgAN patients. These conditions bring about a relatively important window for understanding the pathogenesis of IgAN. Gd-IgA1 is the core of the pathogenesis of IgAN. Most IgA is produced at mucosal sites; however, antigen-activated Toll-like receptor activation pathways expressed by antigen-presenting cells and B-cell homing receptors are different in the intestinal and respiratory mucosa, and the link between respiratory and intestinal mucosa is not well understood in the pathogenesis of IgAN. Budesonide treatment of IgAN is thought to inhibit the intestinal immune response by binding to glucocorticoid receptors in the intestinal mucosa or submucosa; however, it is unclear whether there is a therapeutic effect in respiratory mucosa-derived IgA nephropathy. The present review firstly described the relationship between the gut and respiratory mucosa, and the differences in antigen-presenting cell activation pathways and B-cell homing from the perspective of COVID-19 vaccines.