{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,15]],"date-time":"2026-08-15T17:27:14Z","timestamp":1786814834905,"version":"build-2736575974"},"reference-count":35,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T00:00:00Z","timestamp":1784678400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T00:00:00Z","timestamp":1784678400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82003905"],"award-info":[{"award-number":["82003905"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82471849"],"award-info":[{"award-number":["82471849"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2026,7,31]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The spleen plays a significant role in hepatic fibrosis progression. B cells are the main splenic lymphocytes, but their specific contributions and underlying mechanisms remain unclear. Hepatic fibrosis was induced in mice by intraperitoneal administration of carbon tetrachloride (CCl\n                    <jats:sub>4<\/jats:sub>\n                    ). Splenectomy or sham operation was performed during the fibrotic process. Hepatic fibrosis severity and the proportion of splenic B cells were assessed. Splenic B cells isolated from fibrotic and control mice underwent mRNA sequencing. Protein expression of phosphorylated\u2010p38 MAPK (p\u2010p38 MAPK), total p38 MAPK, phosphorylated\u2010NF\u2010\u03baB p65 (p\u2010NF\u2010\u03baB p65), and total NF\u2010\u03baB p65 were determined by Western blotting using total protein extracted from the splenic B cells. Signal transduction pathways were investigated in isolated splenic B cells to elucidate mechanisms of phenotypic alteration. CCl\n                    <jats:sub>4<\/jats:sub>\n                    \u2010induced hepatic fibrosis was associated with B\u2010cell accumulation in both the liver and spleen. Compared with the splenectomized mice, sham\u2010operated fibrotic mice exhibited a higher proportion of hepatic B cells and more severe liver fibrosis. Splenic B cells from fibrotic mice showed an expansion of the IL\u20106\u2010producing subset and elevated expression of pro\u2010inflammatory cytokines. Moreover, splenectomy reduced the proportion of B cells within the fibrotic liver. Splenic B cells from fibrotic mice displayed upregulated expression of p\u2010p38 MAPK and p\u2010NF\u2010\u03baB p65. In CCl\n                    <jats:sub>4<\/jats:sub>\n                    \u2010induced hepatic fibrosis, splenic B cells accumulate and adopt a pro\u2010inflammatory phenotype. This shift, mediated through activation of the p38 MAPK\/NF\u2010\u03baB signaling pathway, promotes hepatic fibrosis progression. These findings identify splenic B cells as potential therapeutic targets for managing liver disease.\n                  <\/jats:p>","DOI":"10.1096\/fj.202601010r","type":"journal-article","created":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T15:23:29Z","timestamp":1784733809000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Splenic B Cells Accumulate and Adopt a Pro\u2010Inflammatory Phenotype to Accelerate Fibrosis in a\n                    <scp>CCl<\/scp>\n                    <sub>4<\/sub>\n                    \u2010Induced Liver Fibrosis Model"],"prefix":"10.1096","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4217-4343","authenticated-orcid":false,"given":"Keping","family":"Feng","sequence":"first","affiliation":[{"name":"Department of General Surgery, National\u2010Local Joint Engineering Research Center of Biodiagnostic &amp; Biotherapy The Second Affiliated Hospital of Xi'an 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