Purchase this article with an account.
R. W. Read, S. D. Vogt, S. R. Barnum; Absence of Anaphylatoxin Receptors Exacerbates Experimental Autoimmune Uveitis. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2656.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Previous studies have shown that deficiency in the central components of complement activation or inhibition of that activation reduces the severity of disease in experimental autoimmune uveitis (EAU). Surprisingly, however, independent deletion of receptors for the anaphylatoxins showed no effect on EAU severity. The current study was carried out to determine the effect of a simultaneous genetic deficiency of both receptors for the complement anaphylatoxins, C3aR and C5aR, on EAU.
C57BL/6 mice deficient in one each of the receptors for the anaphylatoxins C3a or C5a (C3aR-KO and C5aR-KO, respectively) were crossed to produce double receptor knock out mice. These mice were phenotypically indistinguishable from wild type mice with regard to ocular anatomy. Double receptor knock out and wild type mice were induced for EAU with a peptide of amino acids 1-20 of human IRBP in complete Freund's adjuvant with concurrent pertussis toxin. At 21 days post induction, eyes were enucleated and snap frozen in OCT. 10 micron sections were stained with H&E and 6 equidistant planes through the eye rated for the severity of EAU by a single masked grader, on a ordinal scale from 0 to 4 in 1/2 point increments. Mean scores from each animal were used in a student t-test to compare severity of disease between groups.
Mice deficient in both receptors for the anaphylatoxins exhibited more severe disease than did wild type mice (mean disease severities for wild type and double receptor knock out mice, 0.22 and 0.48, respectively)(p = 0.028).
This PDF is available to Subscribers Only