Building on prior observations that IBD patients harbor numerous taxa with elevated IgA coating [32] and that UC patient-derived fecal EVs contribute to mucosal immune dysregulation [33], we show that L. johnsonii-EVs downregulate epithelial pIgR and FcRn, reducing luminal IgA and IgG transcytosis and normalizing bacterial immune targeting. Here, FCGRT is linked to inflammatory bowel disease.