Dissemin is shutting down on January 1st, 2025

Published in

Elsevier, Immunology Letters, 2(160), p. 163-171

DOI: 10.1016/j.imlet.2014.01.014

Links

Tools

Export citation

Search in Google Scholar

Autoantibodies to complement components in C3 glomerulopathy and atypical hemolytic uremic syndrome.

This paper is available in a repository.
This paper is available in a repository.

Full text: Download

Green circle
Preprint: archiving allowed
Red circle
Postprint: archiving forbidden
Red circle
Published version: archiving forbidden
Data provided by SHERPA/RoMEO

Abstract

The alternative pathway of complement is implicated in the pathogenesis of several renal diseases, such as atypical hemolytic uremic syndrome, dense deposit disease and other forms of C3 glomerulopathy. The underlying complement defects include genetic and/or acquired factors, the latter in the form of autoantibodies. Because the autoimmune forms require a specific treatment, in part different from that of the genetic forms, it is important to detect the autoantibodies as soon as possible and understand their characteristics. In this overview, we summarize the types of anti-complement autoantibodies detected in such diseases, i.e. autoantibodies to factor H, factor I, C3b, factor B and those against the C3 convertases (C3 nephritic factor and C4 nephritic factor). We draw attention to newly described autoantibodies and their characteristics, and highlight similarities and differences in the autoimmune forms of these diseases.