POBS relieves antigen-induced experimental Sjögren’s syndrome by regulating B lymphocyte subsets via CXCL13/CXCR5 signaling pathway

Primary Sjögren’s syndrome (pSS) is an autoimmune disorder characterized by lymphocyte infiltration into exocrine glands, leading to dry eyes and mouth. Its pathogenesis involves B cell hyperactivity and type I interferon activation. CXCL13 promotes B cell migration and ectopic germinal center formation in target tissues. This study investigated whether paeoniflorin-6′-O-benzene sulfonate (POBS) alleviates experimental Sjögren’s syndrome (ESS) by modulating B cell subsets via the CXCL13/CXCR5 pathway. Altered B cell subsets were observed in pSS patient blood and labial glands, suggesting memory B cell migration. In SG-protein immunized ESS mice, POBS reduced lymphocyte infiltration in submandibular glands, suppressed splenic B cell activation, and modulated peripheral B cell subpopulations. POBS also downregulated CXCL13 and CXCR5 expression. These results demonstrate that POBS attenuates gland damage and immune infiltration by regulating B cells via CXCL13/CXCR5, indicating its therapeutic potential for pSS.