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Article: Systemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strains

TitleSystemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strains
Authors
KeywordsApoptotic cells
Autoimmunity
Dendritic cells
Lupus
Necrotic cells
Issue Date2005
PublisherWiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.eji.de
Citation
European Journal Of Immunology, 2005, v. 35 n. 11, p. 3364-3375 How to Cite?
AbstractSystemic lupus erythematosus (SLE) is an autoimmune disorder of a largely unknown etiology. Anti-double-stranded (ds) DNA antibodies are a classic hallmark of the disease, although the mechanism underlying their induction remains unclear. We demonstrate here that, in both lupus-prone and normal mouse strains, strong anti-dsDNA antibody responses can be induced by dendritic cells (DC) that have ingested syngeneic necrotic (DC/nec), but not apoptotic (DC/apo), cells. Clinical manifestations of lupus were evident, however, only in susceptible mouse strains, which correlate with the ability of DC/nec to release IFN-γ and to induce the pathogenic IgG2a anti-dsDNA antibodies. Injection of DC/nec not only accelerated disease progression in the MRL/MpJ-lpr/lpr lupus-prone mice but also induced a lupus-like disease in the MRL/MpJ-+/+ wild-type control strain. Immune complex deposition was readily detectable in the kidneys, and the mice developed proteinuria. Strikingly, female MRL/MpJ-+/+ mice that had received DC/nec, but not DC/apo, developed a 'butterfly' facial lesion resembling a cardinal feature of human SLE. Our study therefore demonstrates that DC/nec inducing a Th1 type of responses, which are otherwise tightly regulated in a normal immune system, may play a pivotal role in SLE pathogenesis. © 2005 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.
Persistent Identifierhttp://hdl.handle.net/10722/48618
ISSN
2015 Impact Factor: 4.179
2015 SCImago Journal Rankings: 2.568
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMa, Len_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorTrendellSmith, NJen_HK
dc.contributor.authorWu, Aen_HK
dc.contributor.authorTian, Len_HK
dc.contributor.authorLam, ACen_HK
dc.contributor.authorChan, AKen_HK
dc.contributor.authorLo, CKen_HK
dc.contributor.authorChik, Sen_HK
dc.contributor.authorKo, KHen_HK
dc.contributor.authorTo, CKWen_HK
dc.contributor.authorKam, SKen_HK
dc.contributor.authorLi, XSen_HK
dc.contributor.authorYang, CHen_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorNg, MHen_HK
dc.contributor.authorStott, DIen_HK
dc.contributor.authorMacPherson, GGen_HK
dc.contributor.authorHuang, FPen_HK
dc.date.accessioned2008-05-22T04:19:11Z-
dc.date.available2008-05-22T04:19:11Z-
dc.date.issued2005en_HK
dc.identifier.citationEuropean Journal Of Immunology, 2005, v. 35 n. 11, p. 3364-3375en_HK
dc.identifier.issn0014-2980en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48618-
dc.description.abstractSystemic lupus erythematosus (SLE) is an autoimmune disorder of a largely unknown etiology. Anti-double-stranded (ds) DNA antibodies are a classic hallmark of the disease, although the mechanism underlying their induction remains unclear. We demonstrate here that, in both lupus-prone and normal mouse strains, strong anti-dsDNA antibody responses can be induced by dendritic cells (DC) that have ingested syngeneic necrotic (DC/nec), but not apoptotic (DC/apo), cells. Clinical manifestations of lupus were evident, however, only in susceptible mouse strains, which correlate with the ability of DC/nec to release IFN-γ and to induce the pathogenic IgG2a anti-dsDNA antibodies. Injection of DC/nec not only accelerated disease progression in the MRL/MpJ-lpr/lpr lupus-prone mice but also induced a lupus-like disease in the MRL/MpJ-+/+ wild-type control strain. Immune complex deposition was readily detectable in the kidneys, and the mice developed proteinuria. Strikingly, female MRL/MpJ-+/+ mice that had received DC/nec, but not DC/apo, developed a 'butterfly' facial lesion resembling a cardinal feature of human SLE. Our study therefore demonstrates that DC/nec inducing a Th1 type of responses, which are otherwise tightly regulated in a normal immune system, may play a pivotal role in SLE pathogenesis. © 2005 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.en_HK
dc.format.extent1586594 bytes-
dc.format.extent657705 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.languageengen_HK
dc.publisherWiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.eji.deen_HK
dc.relation.ispartofEuropean Journal of Immunologyen_HK
dc.rightsPublished in European Journal of Immunology, 2005, v. 35 n. 11, p. 3364-3375en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectApoptotic cellsen_HK
dc.subjectAutoimmunityen_HK
dc.subjectDendritic cellsen_HK
dc.subjectLupusen_HK
dc.subjectNecrotic cellsen_HK
dc.titleSystemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strainsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-2980&volume=35&issue=11&spage=3364&epage=3375&date=2005&atitle=Systemic+autoimmune+disease+induced+by+dendritic+cells+that+have+captured+necrotic+but+not+apoptotic+cells+in+susceptible+mouse+strainsen_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.emailLeung, SY:suetyi@hkucc.hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1002/eji.200535192en_HK
dc.identifier.pmid16224814-
dc.identifier.scopuseid_2-s2.0-27944460001en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27944460001&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume35en_HK
dc.identifier.issue11en_HK
dc.identifier.spage3364en_HK
dc.identifier.epage3375en_HK
dc.identifier.isiWOS:000233522400029-
dc.publisher.placeGermanyen_HK

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