edoc

Anti-C1q autoantibodies from systemic lupus erythematosus patients activate the complement system via both the classical and lectin pathways

Thanei, Sophia and Vanhecke, Dominique and Trendelenburg, Marten. (2015) Anti-C1q autoantibodies from systemic lupus erythematosus patients activate the complement system via both the classical and lectin pathways. Clinical Immunology , 160 (2). pp. 180-187.

Full text not available from this repository.

Official URL: https://edoc.unibas.ch/62491/

Downloads: Statistics Overview

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.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Clinical Immunology (Trendelenburg)
UniBasel Contributors:Trendelenburg, Marten
Item Type:Article, refereed
Article Subtype:Research Article
ISSN:1521-6616
e-ISSN:1521-7035
Note:Publication type according to Uni Basel Research Database: Journal article
Identification Number:
Last Modified:20 Nov 2018 16:28
Deposited On:20 Nov 2018 16:28

Repository Staff Only: item control page