ArticleMolecular immunology
Suppression of complement activation by recombinant Crry inhibits experimental autoimmune anterior uveitis (EAAU).
Article in Molecular immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Correlation of Circulating Complement Levels with Clinical Characteristics of Patients with Diabetic Retinopathy.International journal of general medicine · 2024Article
- Therapeutic Effects of Upadacitinib on Experimental Autoimmune Uveitis: Insights From Single-Cell Analysis.Investigative ophthalmology & visual science · 2023Article
- Exploring the involvement of the alternative complement pathway in non-infectious uveitis pathogenesis.Frontiers in immunology · 2023Article
- Article
- Autoimmune uveitis: clinical, pathogenetic, and therapeutic features.Clinical and experimental medicine · 2016Review
- Complement anaphylatoxin receptors C3aR and C5aR are required in the pathogenesis of experimental autoimmune uveitis.Journal of leukocyte biology · 2016Article
- Chitosan oligosaccharides attenuate ocular inflammation in rats with experimental autoimmune anterior uveitis.Mediators of inflammation · 2014Article
- The future of uveitis treatment.Ophthalmology · 2014Review
- Inhibition of complement alternative pathway suppresses experimental autoimmune anterior uveitis by modulating T cell responses.The Journal of biological chemistry · 2011Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
This study was initiated to explore the effect of recombinant rat Crry linked to the Fc portion of rat IgG2a (Crry-Ig) on the induction of experimental autoimmune anterior uveitis (EAAU) and on established disease. EAAU was induced in Lewis rats by immunization with bovine melanin-associated antigen (MAA). MAA sensitized animals received Crry-Ig, rat IgG2a (isotype control) or PBS separately before the onset of EAAU or after the onset of clinical disease. Administration of Crry-Ig suppressed the induction of EAAU while all animals injected with IgG2a or PBS developed the normal course of EAAU. Treatment with Crry-Ig resulted in the suppression of ocular complement activation as well as the functional activity of complement in the peripheral blood. At the peak of EAAU, levels of IFN-γ, IP-10, ICAM-1 and LECAM-1 were significantly reduced within the eyes of Crry-Ig treated Lewis rats. Importantly, administration of Crry-Ig even after the onset of EAAU resulted in a sharp decline in the disease activity and early resolution of EAAU. Collectively, the evidence presented here demonstrate that inhibition of complement by Crry-Ig results in low levels of inflammatory molecules-C3 activation products, MAC, cytokines, chemokines and adhesion molecules in the eye. Down-regulation of these molecules affects the infiltration and recruitment of inflammatory cells to the eye resulting in the inhibition of EAAU.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.