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Complement Factor H-Related 3 Enhanced Inflammation and Complement Activation in Human RPE Cells.

Nicole Schäfer1,2, Anas Rasras3,4, Delia M Ormenisan1

  • 1Department of Ophthalmology, University Hospital Regensburg, Regensburg, Germany.

Frontiers in Immunology
|November 25, 2021
PubMed
Summary

Complement Factor H-Related 3 (FHR-3) triggers local complement activation within retinal cells, driving inflammation. Targeting FHR-3 may offer new therapies for degenerative diseases like AMD.

Keywords:
AMDFHR-3RETC-2RPE cells FHR-3 alters RPE cell complosomecomplement activationcomplosomeinflammationoxidative stress epitopes

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Area of Science:

  • Immunology
  • Ophthalmology
  • Cell Biology

Background:

  • Complement Factor H-Related 3 (FHR-3) is a key regulator of the complement system.
  • Its local, cellular functions, particularly in diseases like age-related macular degeneration (AMD), are not well understood.

Purpose of the Study:

  • To investigate the non-canonical cellular functions of FHR-3 in retinal pigment epithelium (RPE) cells.
  • To explore FHR-3 as a potential therapeutic target for degenerative diseases.

Main Methods:

  • Studied FHR-3 interaction with oxidative stress epitopes and complement factor H (FH).
  • Assessed FHR-3 internalization by RPE cells and its effect on complement component and receptor expression.
  • Analyzed complement activation products, inflammasome activation, and cytokine secretion.
  • Evaluated the therapeutic potential of an anti-FHR-3 antibody (RETC-2-ximab).

Main Results:

  • FHR-3 binds to oxidative stress sites and competes with FH.
  • FHR-3 is internalized by RPE cells, modulating complement components (C3, FB) and receptors (C3aR, CR3).
  • FHR-3 induces intracellular complement activation, C3a translocation, NLRP3 inflammasome activation, and pro-inflammatory cytokine release (IL-1ß, IL-18, IL-6, TNF-α).
  • The anti-FHR-3 antibody RETC-2-ximab mitigated FHR-3 effects on ARPE-19 cells.

Conclusions:

  • FHR-3 acts as an exogenous trigger for the RPE cell "complosome."
  • FHR-3 promotes a pro-inflammatory microenvironment in RPE cells.
  • FHR-3 is a potential therapeutic target for degenerative diseases associated with complement dysregulation.