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Article: Pathogenesis of systemic lupus erythematosus

TitlePathogenesis of systemic lupus erythematosus
Authors
Issue Date2003
PublisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/
Citation
Journal Of Clinical Pathology, 2003, v. 56 n. 7, p. 481-490 How to Cite?
AbstractThe exact patho-aetiology of systemic lupus erythematosus (SLE) remains elusive. An extremely complicated and multifactorial interaction among various genetic and environmental factors is probably involved. Multiple genes contribute to disease susceptibility. The interaction of sex, hormonal milieu, and the hypothalamo-pituitary-adrenal axis modifies this susceptibility and the clinical expression of the disease. Defective immune regulatory mechanisms, such as the clearance of apoptotic cells and immune complexes, are important contributors to the development of SLE. The loss of immune tolerance, increased antigenic load, excess T cell help, defective B cell suppression, and the shifting of T helper 1 (Th1) to Th2 immune responses leads to B cell hyperactivity and the production of pathogenic autoantibodies. Finally, certain environmental factors are probably required to trigger the disease.
Persistent Identifierhttp://hdl.handle.net/10722/42158
ISSN
2015 Impact Factor: 2.912
2015 SCImago Journal Rankings: 1.260
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMok, CCen_HK
dc.contributor.authorLau, CSen_HK
dc.date.accessioned2007-01-08T02:30:29Z-
dc.date.available2007-01-08T02:30:29Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Clinical Pathology, 2003, v. 56 n. 7, p. 481-490en_HK
dc.identifier.issn0021-9746en_HK
dc.identifier.urihttp://hdl.handle.net/10722/42158-
dc.description.abstractThe exact patho-aetiology of systemic lupus erythematosus (SLE) remains elusive. An extremely complicated and multifactorial interaction among various genetic and environmental factors is probably involved. Multiple genes contribute to disease susceptibility. The interaction of sex, hormonal milieu, and the hypothalamo-pituitary-adrenal axis modifies this susceptibility and the clinical expression of the disease. Defective immune regulatory mechanisms, such as the clearance of apoptotic cells and immune complexes, are important contributors to the development of SLE. The loss of immune tolerance, increased antigenic load, excess T cell help, defective B cell suppression, and the shifting of T helper 1 (Th1) to Th2 immune responses leads to B cell hyperactivity and the production of pathogenic autoantibodies. Finally, certain environmental factors are probably required to trigger the disease.en_HK
dc.format.extent179608 bytes-
dc.format.extent110770 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/pdf-
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/en_HK
dc.relation.ispartofJournal of Clinical Pathologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsJournal of Clinical Pathology. Copyright © B M J Publishing Group.en_HK
dc.subject.meshAntibody formationen_HK
dc.subject.meshAutoantibodies - immunologyen_HK
dc.subject.meshB-lymphocytesen_HK
dc.subject.meshCytokinesen_HK
dc.subject.meshLupus erythematosus, systemicen_HK
dc.titlePathogenesis of systemic lupus erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9746&volume=56&issue=7&spage=481&epage=490&date=2003&atitle=Pathogenesis+of+systemic+lupus+erythematosusen_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.authorityLau, CS=rp01348en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/jcp.56.7.481en_HK
dc.identifier.pmid12835292en_HK
dc.identifier.pmcidPMC1769989-
dc.identifier.scopuseid_2-s2.0-0037668545en_HK
dc.identifier.hkuros95757-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037668545&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume56en_HK
dc.identifier.issue7en_HK
dc.identifier.spage481en_HK
dc.identifier.epage490en_HK
dc.identifier.isiWOS:000183883500001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridMok, CC=7102344226en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK
dc.identifier.citeulike3421353-

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