Defective prevention of immune precipitation in autoimmune diseases is independent of C4A*Q0

2.50
Hdl Handle:
http://hdl.handle.net/2336/53293
Title:
Defective prevention of immune precipitation in autoimmune diseases is independent of C4A*Q0
Authors:
Arason, G J; Kolka, R; Hreidarsson, A B; Gudjonsson, H; Schneider, P M; Fry, L; Arnason, A
Citation:
Clin. Exp. Immunol. 2005, 140(3):572-9
Issue Date:
1-Jun-2005
Abstract:
Increased prevalence of C4 null alleles is a common feature of autoimmune diseases. We have shown previously that complement-dependent prevention of immune precipitation (PIP) is defective in patients with systemic lupus erythematosus (SLE), and correlated this defect with C4A*Q0 and low levels of the C4A isotype. To further clarify the role of C4A in the aetiology of SLE, we now extend our studies to other diseases which have been associated with C4A*Q0. The frequency of C4A*Q0 was increased in Icelandic patients with coeliac disease (0.50; P < 0.001), Grave's disease (0.30; P = 0.002) and insulin-dependent diabetes mellitus (0.23; P = 0.04) and in British patients with dermatitis herpetiformis (0.42; P = 0.002) and this was reflected in low levels of C4A. In spite of this, PIP was normal in these patients, and in marked contrast to our previous observations on connective tissue diseases, PIP measurements in these patient groups correlated more strongly with levels of C4B (r = 0.51, P = 0.0000004) than C4A. Patients with increased levels of anti-C1q antibodies had significantly lower PIP than patients without such antibodies (P < 0.01) and a negative association of PIP with anti-C1q antibodies was also reflected in an increased prevalence (P = 0.006) and levels (P = 0.006) of anti-C1q antibodies in patients with subnormal PIP, as well as a negative correlation between PIP and anti-C1q antibodies (r = - 0.25, P = 0.02). These results show that the PIP defect cannot be explained by low levels of C4A alone and suggest that measurements of anti-C1q antibodies may be useful in future studies on the molecular cause of the PIP defect in autoimmune connective tissue disease.
Description:
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Additional Links:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1809379

Full metadata record

DC FieldValue Language
dc.contributor.authorArason, G J-
dc.contributor.authorKolka, R-
dc.contributor.authorHreidarsson, A B-
dc.contributor.authorGudjonsson, H-
dc.contributor.authorSchneider, P M-
dc.contributor.authorFry, L-
dc.contributor.authorArnason, A-
dc.date.accessioned2009-03-09T13:34:44Z-
dc.date.available2009-03-09T13:34:44Z-
dc.date.issued2005-06-01-
dc.date.submitted2009-03-09-
dc.identifier.citationClin. Exp. Immunol. 2005, 140(3):572-9en
dc.identifier.issn0009-9104-
dc.identifier.pmid15932521-
dc.identifier.doi10.1111/j.1365-2249.2005.02794.x-
dc.identifier.urihttp://hdl.handle.net/2336/53293-
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractIncreased prevalence of C4 null alleles is a common feature of autoimmune diseases. We have shown previously that complement-dependent prevention of immune precipitation (PIP) is defective in patients with systemic lupus erythematosus (SLE), and correlated this defect with C4A*Q0 and low levels of the C4A isotype. To further clarify the role of C4A in the aetiology of SLE, we now extend our studies to other diseases which have been associated with C4A*Q0. The frequency of C4A*Q0 was increased in Icelandic patients with coeliac disease (0.50; P < 0.001), Grave's disease (0.30; P = 0.002) and insulin-dependent diabetes mellitus (0.23; P = 0.04) and in British patients with dermatitis herpetiformis (0.42; P = 0.002) and this was reflected in low levels of C4A. In spite of this, PIP was normal in these patients, and in marked contrast to our previous observations on connective tissue diseases, PIP measurements in these patient groups correlated more strongly with levels of C4B (r = 0.51, P = 0.0000004) than C4A. Patients with increased levels of anti-C1q antibodies had significantly lower PIP than patients without such antibodies (P < 0.01) and a negative association of PIP with anti-C1q antibodies was also reflected in an increased prevalence (P = 0.006) and levels (P = 0.006) of anti-C1q antibodies in patients with subnormal PIP, as well as a negative correlation between PIP and anti-C1q antibodies (r = - 0.25, P = 0.02). These results show that the PIP defect cannot be explained by low levels of C4A alone and suggest that measurements of anti-C1q antibodies may be useful in future studies on the molecular cause of the PIP defect in autoimmune connective tissue disease.en
dc.language.isoenen
dc.publisherBlackwell Scientific Publicationsen
dc.relation.urlhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1809379en
dc.subject.meshAdolescenten
dc.subject.meshAdulten
dc.subject.meshAgeden
dc.subject.meshAged, 80 and overen
dc.subject.meshAntigen-Antibody Complexen
dc.subject.meshAutoantibodiesen
dc.subject.meshAutoimmune Diseasesen
dc.subject.meshCeliac Diseaseen
dc.subject.meshComplement C1qen
dc.subject.meshComplement C3en
dc.subject.meshComplement C4aen
dc.subject.meshComplement C4ben
dc.subject.meshComplement Hemolytic Activity Assayen
dc.subject.meshDermatitis Herpetiformisen
dc.subject.meshDiabetes Mellitus, Type 1en
dc.subject.meshFemaleen
dc.subject.meshGraves Diseaseen
dc.subject.meshHumansen
dc.subject.meshMaleen
dc.subject.meshMiddle Ageden
dc.titleDefective prevention of immune precipitation in autoimmune diseases is independent of C4A*Q0en
dc.typeArticleen
dc.contributor.departmentDepartment of Immunology, Institute of Laboratory Medicine, Reykjavik, Iceland. garason@landspitali.isen
dc.identifier.journalClinical and experimental immunologyen

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