{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T01:11:50Z","timestamp":1780103510789,"version":"3.54.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2018,10,9]],"date-time":"2018-10-09T00:00:00Z","timestamp":1539043200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2018,10,9]],"date-time":"2018-10-09T00:00:00Z","timestamp":1539043200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2018,11]]},"abstract":"<jats:p>The primary function of myeloid\u2010derived suppressor cells (MDSCs) is reflected in their immune modulatory role in several immune\u2010mediated diseases. In immunoglobulin G4 (IgG4)\u2013related disease (IgG4\u2010RD), it has been hypothesized that there are selective regulatory defects that lead to a T helper 2 (Th2) bias immune response. Herein we have taken advantage of a large cohort of patients with IgG4\u2010related sclerosing cholangitis (IgG4\u2010SC), the most common extrapancreatic involvement of IgG4\u2010RD, as well as controls consisting of primary sclerosing cholangitis, autoimmune hepatitis, and healthy volunteers, to study MDSCs. We report dramatically increased levels of receptor activator for nuclear factor kappa B ligand (RANKL) expression in serum and liver from patients with IgG4\u2010SC compared to both liver\u2010disease and healthy controls. Moreover, in IgG4\u2010SC liver, RANKL\u2010secreting cells specifically colocalized with cluster of differentiation 38\u2013positive plasma cells and MDSCs, particularly monocytic MDSCs, and express the RANKL receptor in liver. Similarly, the frequency and number of peripheral blood MDSCs were significantly increased. Importantly, serum expression levels of RANKL were inversely correlated with the serum level of gamma\u2010glutamyltransferase but significantly positively correlated with the frequency of MDSCs. Moreover, we confirmed that RANKL induced the expansion and activation of MDSCs through the RANKL\/RANK\/nuclear factor kappa B signal pathway. Of note, RANKL\u2010treated MDSCs suppressed T\u2010cell proliferation and induced Th2 differentiation. <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic> Our data suggest that plasma cell\u2013derived RANKL induces the expansion and activation of MDSCs, which suppress T\u2010cell proliferation and contribute to the Th2\u2010type response characteristic of IgG4\u2010SC.<\/jats:p>","DOI":"10.1002\/hep.30095","type":"journal-article","created":{"date-parts":[[2018,5,18]],"date-time":"2018-05-18T08:39:17Z","timestamp":1526632757000},"page":"1922-1936","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":17,"title":["The Immunobiology of Receptor Activator for Nuclear Factor Kappa B Ligand and Myeloid\u2010Derived Suppressor Cell Activation in Immunoglobulin G4\u2013Related Sclerosing Cholangitis"],"prefix":"10.1097","volume":"68","author":[{"given":"Min","family":"Lian","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health; State Key Laboratory for Oncogenes and Related Genes, Renji Hospital; School of Medicine,Shanghai Jiao Tong University; and Shanghai Institute of Digestive Disease,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qixia","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health; State Key Laboratory for Oncogenes and Related Genes, Renji Hospital; School of Medicine,Shanghai Jiao Tong University; and Shanghai Institute of Digestive Disease,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiang","family":"Jiang","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health; State Key Laboratory for Oncogenes and Related Genes, Renji Hospital; School of Medicine,Shanghai Jiao Tong University; and Shanghai Institute of Digestive Disease,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health; 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