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Updated: May 7, 2026

Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
The complement anaphylatoxin receptors are not required for the development of experimental autoimmune uveitis
Russell W Read1, Susan D Vogt, Scott R Barnum
1Department of Ophthalmology, The University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294-1150, USA; Department of Pathology, The University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294-1150, USA; Department of Microbiology, The University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294-1150, USA.
Abstract:
To determine if complement anaphylatoxin-mediated inflammation contributes to the development and progression of experimental autoimmune uveitis (EAU), we induced disease in wild type and complement anaphylatoxin receptor-deficient mice (C3a receptor(-/-), C5a receptor(-/-) and C3aR(-/-)/C5aR(-/-)) and evaluated the eyes three weeks post-induction. No differences in disease severity or in disease incidence were seen between wild type controls and anaphylatoxin receptor-deficient mice. Our data indicate that C3a and C5a-mediated functions are not critical to the development of EAU.
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