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Article: Endothelial cell binding by human polyclonal anti-DNA antibodies: Relationship to disease activity and endothelial functional alterations

TitleEndothelial cell binding by human polyclonal anti-DNA antibodies: Relationship to disease activity and endothelial functional alterations
Authors
Keywordsadhesion molecule
anti-DNA antibody
endothelial cell
von Willebrand factor
Issue Date1995
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEI
Citation
Clinical And Experimental Immunology, 1995, v. 100 n. 3, p. 506-513 How to Cite?
AbstractPolyclonal anti-dsDNA and anti-ssDNA antibodies (PoAb) that showed significant binding to human umbilical vein endothelial cells (HUVEC) were isolated from eight patients with systemic lupus erythematosus (SLE). Anti-dsDNA PoAbs from five patients and anti-ssDNA PoAbs from seven patients demonstrated enhanced binding to HUVEC during active disease, compared with PoAbs obtained from corresponding patients during remission. Reduction of the DNA content in the PoAb preparations by DNase treatment was associated with enhanced binding to HUVEC in 20 of 32 PoAbs tested, which included 75% 'active disease' PoAbs, and with reduced binding to HUVEC in three of 32 PoAbs tested, all obtained during remission. Such altered endothelial cell binding was reversed with DNA reconstitution. Binding of the remaining nine PoAbs to HUVEC was not altered by variations in their DNA content. Induced plasma membrane expression of E-selectin, but reduced expression of vascular cell adhesion molecule-1 (VCAM-1) by HUVEC, was observed following incubation of HUVEC with 'active disease' PoAbs from three and two of the eight patients, respectively. PoAbs and serum samples from two of the eight patients during active disease induced von Willebrand factor release from HUVEC, which was not observed during remission. We conclude that anti-DNA antibodies from selected patients with SLE can bind to endothelial cells. Correlation between cellular binding and disease activity suggests that such binding of anti-DNA antibodies to endothelial cells could be of pathogenic significance. Preliminary data also suggest that the expression of adhesion molecules and haemostatic factor(s) by endothelial cells may be modified following their binding by anti-DNA antibodies.
Persistent Identifierhttp://hdl.handle.net/10722/49105
ISSN
2015 Impact Factor: 3.148
2015 SCImago Journal Rankings: 1.369
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, TMen_HK
dc.contributor.authorYu, PMen_HK
dc.contributor.authorTsang, KLCen_HK
dc.contributor.authorCheng, IKPen_HK
dc.date.accessioned2008-06-12T06:34:32Z-
dc.date.available2008-06-12T06:34:32Z-
dc.date.issued1995en_HK
dc.identifier.citationClinical And Experimental Immunology, 1995, v. 100 n. 3, p. 506-513en_HK
dc.identifier.issn0009-9104en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49105-
dc.description.abstractPolyclonal anti-dsDNA and anti-ssDNA antibodies (PoAb) that showed significant binding to human umbilical vein endothelial cells (HUVEC) were isolated from eight patients with systemic lupus erythematosus (SLE). Anti-dsDNA PoAbs from five patients and anti-ssDNA PoAbs from seven patients demonstrated enhanced binding to HUVEC during active disease, compared with PoAbs obtained from corresponding patients during remission. Reduction of the DNA content in the PoAb preparations by DNase treatment was associated with enhanced binding to HUVEC in 20 of 32 PoAbs tested, which included 75% 'active disease' PoAbs, and with reduced binding to HUVEC in three of 32 PoAbs tested, all obtained during remission. Such altered endothelial cell binding was reversed with DNA reconstitution. Binding of the remaining nine PoAbs to HUVEC was not altered by variations in their DNA content. Induced plasma membrane expression of E-selectin, but reduced expression of vascular cell adhesion molecule-1 (VCAM-1) by HUVEC, was observed following incubation of HUVEC with 'active disease' PoAbs from three and two of the eight patients, respectively. PoAbs and serum samples from two of the eight patients during active disease induced von Willebrand factor release from HUVEC, which was not observed during remission. We conclude that anti-DNA antibodies from selected patients with SLE can bind to endothelial cells. Correlation between cellular binding and disease activity suggests that such binding of anti-DNA antibodies to endothelial cells could be of pathogenic significance. Preliminary data also suggest that the expression of adhesion molecules and haemostatic factor(s) by endothelial cells may be modified following their binding by anti-DNA antibodies.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEIen_HK
dc.relation.ispartofClinical and Experimental Immunologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsClinical and Experimental Immunology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subjectadhesion moleculeen_HK
dc.subjectanti-DNA antibodyen_HK
dc.subjectendothelial cellen_HK
dc.subjectvon Willebrand factoren_HK
dc.titleEndothelial cell binding by human polyclonal anti-DNA antibodies: Relationship to disease activity and endothelial functional alterationsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-9104&volume=100&issue=3&spage=506&epage=513&date=1995&atitle=Endothelial+cell+binding+by+human+polyclonal+anti-DNA+antibodies:+relationship+to+disease+activity+and+endothelial+functional+alternationsen_HK
dc.identifier.emailChan, TM:dtmchan@hku.hken_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1111/j.1365-2249.1995.tb03730.x-
dc.identifier.pmid7774063-
dc.identifier.pmcidPMC1534478en_HK
dc.identifier.scopuseid_2-s2.0-0029004164en_HK
dc.identifier.hkuros49825-
dc.identifier.volume100en_HK
dc.identifier.issue3en_HK
dc.identifier.spage506en_HK
dc.identifier.epage513en_HK
dc.identifier.isiWOS:A1995RB16300022-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridYu, PM=7403599544en_HK
dc.identifier.scopusauthoridTsang, KLC=7201554745en_HK
dc.identifier.scopusauthoridCheng, IKP=7102537483en_HK

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