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Hui Shao, Guomin Jiang, Yunsong Wang, Xiaomin Zhang, Deming Sun, Henry J Kaplan, Lei Zhou; Dynamic quantitative proteomic analysis of AqH from experimental recurrent autoimmune uveitis . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):889.
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© ARVO (1962-2015); The Authors (2016-present)
The mechanism of recurrent autoimmune uveitis is unknown. We hypothesized that quantitative proteomic analysis of AqH would identify proteins that correlate with recurrent episodes of EAU induced by interphotoreceptor retinoid-binding protein (IRBP)-specific T cells (tEAU) in rats.
tEAU was induced in Lewis rats by injection of IRBP peptide (R16)-specific T cells collected from R16 immunized Lewis rats. Intraocular inflammation was clinically evaluated. AqH samples were collected on days 0 (naïve), 1, 4 (onset), 7 (peak), 11 (remission), 14 (second attack), 24 (second peak) and 30 (second remission), and analyzed by iTRAQ Quantitative Proteomics. AqH samples were pooled from six eyes at each time point and assessed by Spearman correlation coefficient by analyzing the samples in replicates from two independent experiments.
Among ~200 identified AqH proteins (<1% false discovery rate, FDR), 34 were found to correlate with clinical recurrence. Pathway analysis using MetaCore revealed that proteins in all three complement pathways (classical, lectin and alternative) showed the strongest association with intraocular inflammation, with blood coagulation and HDL-mediated reverse cholesterol transport being second and third, respectively. C-reactive protein (CRP), a protein that binds to lysophosphatidylcholine and activates the complement system via the C1Q complex, was increased during inflammatory episodes and subsided during remission.
This study using proteomic analysis in AqH during recurrent EAU induced by uveitogenic T cells in Lewis rats demonstrated the involvement of complement pathways and CRP. However, it is unknown whether complement activation is the initiator or consequence of recurrent intraocular inflammation.
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