A small exploratory study examined whether Epstein-Barr virus (EBV)–associated changes in mucosal B cells could contribute to IgA nephropathy (IgAN). Researchers analyzed breast milk from three mothers with stable IgAN and three healthy controls and found a significantly higher proportion of EBV-positive CD19+ B cells in the IgAN group (30.8% vs 11.3%). EBV-positive migrating pre-plasma cells were also more common in mothers with IgAN, supporting the possibility that EBV infection may be associated with altered B-cell differentiation and mucosal immune responses in the disease.
Additional findings pointed to differences in B-cell trafficking and galactose-deficient IgA1 (Gd-IgA1) biology. B cells from mothers with IgAN showed greater expression of the gut-homing receptor CCR9 and a higher proportion of Gd-IgA1–positive cells with a pre-plasma-cell phenotype, suggesting dysregulated mucosal immune activity. However, the investigators emphasized that the relationship between EBV, altered B-cell localization, Gd-IgA1 production, and kidney injury remains uncertain. Given the extremely small sample size, these findings are hypothesis-generating and require confirmation in substantially larger studies.
Reference: Zachova K, Cutkova A, Kosztyu P, et al. IgA nephropathy-associated breast milk B cell alterations. Front Immunol. 2026 May 8;17:1784598. doi: 10.3389/fimmu.2026.1784598.
