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Article: B1a cells play a pathogenic role in the development of autoimmune arthritis

TitleB1a cells play a pathogenic role in the development of autoimmune arthritis
Authors
KeywordsB1 cell
Receptor activator of nuclear factor kappa-B ligand
Collagen-induced arthritis
Autoimmune disease
Immunology and Microbiology Section
Immune response
Immunity
Issue Date2016
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2016, v. 7 n. 15, p. 19299-19311 How to Cite?
AbstractDysregulated functions of B1 cells have been implicated in the disease progression of various autoimmune disorders, but it remains largely unclear whether B1 cells are involved in the pathogenesis of autoimmune arthritis. In this study, we found that peritoneal B1a cells underwent proliferation and migrated to the inflamed joint tissue with upregulated RANKL expression during collagen-induced arthritis (CIA) development in mice. Adoptive transfer of B1a cells exacerbated arthritic severity and joint damage while intraperitoneal depletion of B1 cells ameliorated both arthritic symptoms and joint pathology in CIA mice. In culture, RANKL-expressing B1a cells significantly promoted the expansion of osteoclasts derived from bone marrow cells, which were in accord with the in vivo findings of increased osteoclastogenesis in CIA mice transferred with B1a cells. Together, these results have demonstrated a pathogenic role of B1a cells in the development of autoimmune arthritis through RANKL-mediated osteoclastogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/232147
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDeng, J-
dc.contributor.authorWang, X-
dc.contributor.authorChen, Q-
dc.contributor.authorSun, X-
dc.contributor.authorXiao, F-
dc.contributor.authorKo, KH-
dc.contributor.authorZhang, M-
dc.contributor.authorLu, L-
dc.date.accessioned2016-09-20T05:28:03Z-
dc.date.available2016-09-20T05:28:03Z-
dc.date.issued2016-
dc.identifier.citationOncotarget, 2016, v. 7 n. 15, p. 19299-19311-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/232147-
dc.description.abstractDysregulated functions of B1 cells have been implicated in the disease progression of various autoimmune disorders, but it remains largely unclear whether B1 cells are involved in the pathogenesis of autoimmune arthritis. In this study, we found that peritoneal B1a cells underwent proliferation and migrated to the inflamed joint tissue with upregulated RANKL expression during collagen-induced arthritis (CIA) development in mice. Adoptive transfer of B1a cells exacerbated arthritic severity and joint damage while intraperitoneal depletion of B1 cells ameliorated both arthritic symptoms and joint pathology in CIA mice. In culture, RANKL-expressing B1a cells significantly promoted the expansion of osteoclasts derived from bone marrow cells, which were in accord with the in vivo findings of increased osteoclastogenesis in CIA mice transferred with B1a cells. Together, these results have demonstrated a pathogenic role of B1a cells in the development of autoimmune arthritis through RANKL-mediated osteoclastogenesis.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectB1 cell-
dc.subjectReceptor activator of nuclear factor kappa-B ligand-
dc.subjectCollagen-induced arthritis-
dc.subjectAutoimmune disease-
dc.subjectImmunology and Microbiology Section-
dc.subjectImmune response-
dc.subjectImmunity-
dc.titleB1a cells play a pathogenic role in the development of autoimmune arthritis-
dc.typeArticle-
dc.identifier.emailWang, X: xiaohuiwang@hku.hk-
dc.identifier.emailKo, KH: khko@hku.hk-
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityWang, X=rp02664-
dc.identifier.authorityLu, L=rp00477-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.18632/oncotarget.8244-
dc.identifier.pmid27014914-
dc.identifier.pmcidPMC4991384-
dc.identifier.scopuseid_2-s2.0-84964797886-
dc.identifier.hkuros264603-
dc.identifier.volume7-
dc.identifier.issue15-
dc.identifier.spage19299-
dc.identifier.epage19311-
dc.identifier.isiWOS:000375804000019-
dc.publisher.placeUnited States-

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