Anti-C1q autoantibodies from systemic lupus erythematosus patients activate the complement system via both the classical and lectin pathways.
Details
Serval ID
serval:BIB_FDD3AB0A5C4C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Anti-C1q autoantibodies from systemic lupus erythematosus patients activate the complement system via both the classical and lectin pathways.
Journal
Clinical Immunology (orlando, Fla.)
ISSN
1521-7035 (Electronic)
ISSN-L
1521-6616
Publication state
Published
Issued date
2015
Peer-reviewed
Oui
Volume
160
Number
2
Pages
180-187
Language
english
Abstract
Autoantibodies against complement C1q (anti-C1q) strongly correlate with the occurrence of lupus nephritis and hypocomplementemia in systemic lupus erythematosus (SLE). Although a direct pathogenic role of anti-C1q has been suggested, the assumed complement-activating capacity remains to be elucidated. Using an ELISA-based assay, we found that anti-C1q activate the classical (CP) and lectin pathways (LP) depending on the anti-C1q immunoglobulin-class repertoire present in the patient's serum. IgG anti-C1q resulted in the activation of the CP as reflected by C4b deposition in the presence of purified C1 and C4 in a dose-dependent manner. The extent of C4b deposition correlated with anti-C1q levels in SLE patients but not in healthy controls. Our data indicate that SLE patient-derived anti-C1q can activate the CP and the LP but not the alternative pathway of complement. These findings are of importance for the understanding of the role of anti-C1q in SLE suggesting a direct link to hypocomplementemia.
Pubmed
Web of science
Create date
27/10/2015 17:23
Last modification date
20/08/2019 16:28