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.)
Author(s)
Thanei S., Vanhecke D., Trendelenburg M.
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
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