POBS Relieves Antigen-Induced Experimental Sjögren's Disease by Regulating B Lymphocyte Subsets via CXCL13/CXCR5 Signaling Pathway.

Abstract

Sjögren's Disease (SjD) 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 Disease (ESjD) by modulating B cell subsets via the CXCL13/CXCR5 pathway. Altered B cell subsets were observed in SjD patient blood and labial glands, suggesting memory B cell migration. In SG-protein immunised ESjD 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 SjD.