Patients with systemic lupus erythematosus are deficient in complement-dependent prevention of immune precipitation.

2.50
Hdl Handle:
http://hdl.handle.net/2336/68393
Title:
Patients with systemic lupus erythematosus are deficient in complement-dependent prevention of immune precipitation.
Authors:
Arason, G J; Steinsson, K; Kolka, R; Víkingsdottir, Th; D'Ambrogio, M S; Valdimarsson, H
Citation:
Rheumatology (Oxford). 2004, 43(6):783-9
Issue Date:
1-Jun-2004
Abstract:
OBJECTIVE: A functional deficiency of complement has been implicated but not conclusively demonstrated in the pathogenesis of systemic lupus erythematosus (SLE). To test this, we studied several aspects of complement in 44 patients with SLE, 46 patients with rheumatoid arthritis and 102 blood donors. METHODS: Prevention of immune precipitation (PIP) was measured by an enzyme immunoassay, levels of C1q, C4 and C3 by rocket immunoelectrophoresis, C4A, C4B and C3d by enzyme-linked immunosorbent assay (ELISA), complement haemolysis (CH50) by standard methods and C4 allotypes by high-voltage agarose electrophoresis and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). RESULTS: PIP was significantly reduced in SLE (P<0.001); the defect was revealed by a sensitive assay measuring this function of complement but not by the other tests employed. The patients were clinically well at the time of study, and levels of C3d, which have been shown to correlate with disease activity, were normal. The defect was more common in patients with early disease (P = 0.009), supporting a role in aetiology or early pathophysiology. PIP was positively correlated with levels of C4 (P = 3 x 10(-5)) and in particular the C4A isotype (P = 9 x 10(-10)) whereas C4B was redundant. CONCLUSIONS: Our results reveal a defect in prevention of immune precipitation in SLE that is apparent at an early stage in the disease and correlates with low levels of C4A. These results indicate that subtle deficiencies of complement may predispose to SLE.
Description:
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Additional Links:
http://rheumatology.oxfordjournals.org/cgi/content/abstract/43/6/783

Full metadata record

DC FieldValue Language
dc.contributor.authorArason, G J-
dc.contributor.authorSteinsson, K-
dc.contributor.authorKolka, R-
dc.contributor.authorVíkingsdottir, Th-
dc.contributor.authorD'Ambrogio, M S-
dc.contributor.authorValdimarsson, H-
dc.date.accessioned2009-05-15T15:22:02Z-
dc.date.available2009-05-15T15:22:02Z-
dc.date.issued2004-06-01-
dc.date.submitted2009-05-15-
dc.identifier.citationRheumatology (Oxford). 2004, 43(6):783-9en
dc.identifier.issn1462-0324-
dc.identifier.pmid15054157-
dc.identifier.doi10.1093/rheumatology/keh183-
dc.identifier.urihttp://hdl.handle.net/2336/68393-
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractOBJECTIVE: A functional deficiency of complement has been implicated but not conclusively demonstrated in the pathogenesis of systemic lupus erythematosus (SLE). To test this, we studied several aspects of complement in 44 patients with SLE, 46 patients with rheumatoid arthritis and 102 blood donors. METHODS: Prevention of immune precipitation (PIP) was measured by an enzyme immunoassay, levels of C1q, C4 and C3 by rocket immunoelectrophoresis, C4A, C4B and C3d by enzyme-linked immunosorbent assay (ELISA), complement haemolysis (CH50) by standard methods and C4 allotypes by high-voltage agarose electrophoresis and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). RESULTS: PIP was significantly reduced in SLE (P<0.001); the defect was revealed by a sensitive assay measuring this function of complement but not by the other tests employed. The patients were clinically well at the time of study, and levels of C3d, which have been shown to correlate with disease activity, were normal. The defect was more common in patients with early disease (P = 0.009), supporting a role in aetiology or early pathophysiology. PIP was positively correlated with levels of C4 (P = 3 x 10(-5)) and in particular the C4A isotype (P = 9 x 10(-10)) whereas C4B was redundant. CONCLUSIONS: Our results reveal a defect in prevention of immune precipitation in SLE that is apparent at an early stage in the disease and correlates with low levels of C4A. These results indicate that subtle deficiencies of complement may predispose to SLE.en
dc.language.isoenen
dc.publisherOxford University Pressen
dc.relation.urlhttp://rheumatology.oxfordjournals.org/cgi/content/abstract/43/6/783en
dc.subject.meshAdulten
dc.subject.meshAgeden
dc.subject.meshAged, 80 and overen
dc.subject.meshAntigen-Antibody Complexen
dc.subject.meshArthritis, Rheumatoiden
dc.subject.meshAutoimmune Diseasesen
dc.subject.meshComplement C4aen
dc.subject.meshComplement Hemolytic Activity Assayen
dc.subject.meshComplement System Proteinsen
dc.subject.meshDisease Progressionen
dc.subject.meshFemaleen
dc.subject.meshHumansen
dc.subject.meshLupus Erythematosus, Systemicen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.titlePatients with systemic lupus erythematosus are deficient in complement-dependent prevention of immune precipitation.en
dc.typeArticleen
dc.contributor.departmentDepartment of Immunology, Institute of Laboratory Medicine, Landspitalinn University Hospital, 101 Reykjavík, Iceland . garason@landspitali.isen
dc.identifier.journalRheumatology (Oxford, England)en

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