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Factor H Autoantibodies and Complement-Mediated Diseases.

Yuzhou Zhang1, Nicolo Ghiringhelli Borsa1, Dingwu Shao1

  • 1Molecular Otolaryngology and Renal Research Laboratories, University of Iowa, Iowa City, IA, United States.

Frontiers in Immunology
|January 1, 2021
PubMed
Summary
This summary is machine-generated.

Autoantibodies targeting Factor H (FH) impair its complement regulation, causing kidney diseases like atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy (C3G). This study identifies FH autoantibody epitopes linked to these conditions.

Keywords:
C3 glomerulopathyatypical hemolytic uremic syndromeautoantibodiescomplementfactor Hmonoclonal gammopathy of renal significance

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Area of Science:

  • Immunology
  • Nephrology
  • Complement System Biology

Background:

  • Factor H (FH) regulates the alternative pathway of complement, preventing tissue damage.
  • Impaired FH function due to autoantibodies causes thrombotic microangiopathies (TMAs) like atypical hemolytic uremic syndrome (aHUS), C3 glomerulopathy (C3G), and monoclonal gammopathy of renal significance (MGRS).
  • FH autoantibodies (FHAAs) exhibit phenotypic variability based on FH domain epitope specificity.

Purpose of the Study:

  • To characterize FH autoantibody (FHAAs) epitopes in patients with TMAs, C3G, or MGRS.
  • To investigate the association between FHAAs, their recognized epitopes, and the genetic deletion of CFHR1 genes.
  • To elucidate the link between diverse autoantibody specificities and disease phenotypes.

Main Methods:

  • Epitope mapping of FHAAs in a patient cohort.
  • Analysis of FH autoantibody prevalence in aHUS, C3G, and MGRS.
  • Correlation of FHAAs with genetic deletions of CFHR1.

Main Results:

  • FH autoantibodies are present in a significant percentage of aHUS and C3G patients.
  • Specific FH epitopes are recognized by FHAAs across different renal diseases.
  • Association observed between FHAAs and the genetic deletion of CFHR1.

Conclusions:

  • FH autoantibodies play a crucial role in the pathogenesis of TMA, C3G, and MGRS.
  • Epitope specificity of FHAAs contributes to disease phenotype variability.
  • Understanding FH autoantibody epitopes and their genetic associations aids in diagnosing and managing these complement-mediated renal diseases.