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Article: Expression and function of TNF family member B cell-activating factor in the development of autoimmune arthritis

TitleExpression and function of TNF family member B cell-activating factor in the development of autoimmune arthritis
Authors
KeywordsApoptosis
Autoimmunity
B lymphocytes
Cytokine
Dendritic cells
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/
Citation
International Immunology, 2005, v. 17 n. 8, p. 1081-1092 How to Cite?
AbstractB cell-activating factor (BAFF), a member of tumor necrosis factor family cytokines, has been shown to enhance the maturation and survival of peripheral B cells. While BAFF is implicated in regulating B cell function and autoimmunity, its role in the development of autoimmune arthritis has not been fully clarified. Using a collagen-induced arthritis (CIA) mouse model, we detected dysregulated expression of BAFF and its receptors in the peripheral lymphoid organs during arthritis induction. Elevated serum levels of BAFF were closely correlated with increased levels of anti-collagen antibodies during the CIA progression. Moreover, dendritic cells (DCs) and macrophages were found to express high amount of BAFF proteins at the acute and chronic stages of CIA, respectively. In cultures, recombinant BAFF suppressed apoptosis of splenic B cells from arthritic mice, and DC-induced B cell proliferation was specifically blocked by soluble decoy receptor B cell maturation antigen-Fc. These findings suggest that overproduction of BAFF by DCs and macrophages may play a crucial role in the pathogenesis of experimental arthritis. © The Japanese Society for Immunology. 2005. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/79103
ISSN
2015 Impact Factor: 3.031
2015 SCImago Journal Rankings: 1.613
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Men_HK
dc.contributor.authorKo, KHen_HK
dc.contributor.authorLam, QLKen_HK
dc.contributor.authorLo, CKCen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorZheng, Ben_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorLu, Len_HK
dc.date.accessioned2010-09-06T07:50:37Z-
dc.date.available2010-09-06T07:50:37Z-
dc.date.issued2005en_HK
dc.identifier.citationInternational Immunology, 2005, v. 17 n. 8, p. 1081-1092en_HK
dc.identifier.issn0953-8178en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79103-
dc.description.abstractB cell-activating factor (BAFF), a member of tumor necrosis factor family cytokines, has been shown to enhance the maturation and survival of peripheral B cells. While BAFF is implicated in regulating B cell function and autoimmunity, its role in the development of autoimmune arthritis has not been fully clarified. Using a collagen-induced arthritis (CIA) mouse model, we detected dysregulated expression of BAFF and its receptors in the peripheral lymphoid organs during arthritis induction. Elevated serum levels of BAFF were closely correlated with increased levels of anti-collagen antibodies during the CIA progression. Moreover, dendritic cells (DCs) and macrophages were found to express high amount of BAFF proteins at the acute and chronic stages of CIA, respectively. In cultures, recombinant BAFF suppressed apoptosis of splenic B cells from arthritic mice, and DC-induced B cell proliferation was specifically blocked by soluble decoy receptor B cell maturation antigen-Fc. These findings suggest that overproduction of BAFF by DCs and macrophages may play a crucial role in the pathogenesis of experimental arthritis. © The Japanese Society for Immunology. 2005. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://intimm.oxfordjournals.org/en_HK
dc.relation.ispartofInternational Immunologyen_HK
dc.rightsInternational Immunology. Copyright © Oxford University Press.en_HK
dc.subjectApoptosisen_HK
dc.subjectAutoimmunityen_HK
dc.subjectB lymphocytesen_HK
dc.subjectCytokineen_HK
dc.subjectDendritic cellsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshArthritis, Experimental - etiology - genetics - immunology - pathologyen_HK
dc.subject.meshAutoantibodies - blooden_HK
dc.subject.meshAutoimmune Diseases - etiology - genetics - immunologyen_HK
dc.subject.meshB-Cell Activating Factoren_HK
dc.subject.meshB-Cell Activation Factor Receptoren_HK
dc.subject.meshB-Lymphocytes - immunology - pathologyen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCollagen - immunologyen_HK
dc.subject.meshDNA, Complementary - geneticsen_HK
dc.subject.meshDendritic Cells - immunologyen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshLymphocyte Activationen_HK
dc.subject.meshMacrophages - immunologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMembrane Proteins - biosynthesis - genetics - immunologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred DBAen_HK
dc.subject.meshRNA, Messenger - genetics - metabolismen_HK
dc.subject.meshReceptors, Tumor Necrosis Factor - biosynthesis - geneticsen_HK
dc.subject.meshTumor Necrosis Factor-alpha - genetics - immunologyen_HK
dc.titleExpression and function of TNF family member B cell-activating factor in the development of autoimmune arthritisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0953-8178&volume=17&issue=8&spage=1081&epage=1092&date=2005&atitle=Expression+and+function+of+TNF+family+member+B+cell-activating+factor+in+the+development+of+autoimmune+arthritisen_HK
dc.identifier.emailLam, QLK: qlam@pathology.hku.hken_HK
dc.identifier.emailSrivastava, G: sgopesh@hkucc.hku.hken_HK
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLam, QLK=rp00312en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityZheng, B=rp00353en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/intimm/dxh287en_HK
dc.identifier.pmid16000326-
dc.identifier.scopuseid_2-s2.0-23844518421en_HK
dc.identifier.hkuros102587en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23844518421&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1081en_HK
dc.identifier.epage1092en_HK
dc.identifier.isiWOS:000230846800010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZhang, M=8416776200en_HK
dc.identifier.scopusauthoridKo, KH=7202688627en_HK
dc.identifier.scopusauthoridLam, QLK=8722491000en_HK
dc.identifier.scopusauthoridLo, CKC=24825171000en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridZheng, B=7201780588en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK
dc.identifier.citeulike269485-

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