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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\u20106\u2032\u2010O\u2010benzene sulfonate (POBS) alleviates Experimental Sj\u00f6gren'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\u2010protein 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.<\/jats:p>","DOI":"10.1002\/iub.70095","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T08:29:17Z","timestamp":1773649757000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>POBS<\/scp>\n                    Relieves Antigen\u2010Induced Experimental\n                    <scp>S<\/scp>\n                    j\u00f6gren's Disease by Regulating\n                    <scp>B<\/scp>\n                    Lymphocyte Subsets via\n                    <scp>CXCL13<\/scp>\n                    \/\n                    <scp>CXCR5<\/scp>\n                    Signaling 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