ArticleJournal of immunology (Baltimore, Md. : 1950)2011
IL-22-induced regulatory CD11b+ APCs suppress experimental autoimmune uveitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy.Frontiers in immunology · 2026Review
- Mice deficient of G-protein coupled receptor 3 (GPR3) developed severe experimental autoimmune uveitis (EAU) through increased effector T cell activities.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis.Molecular and cellular biochemistry · 2024Article
- Interleukin-22 suppresses major histocompatibility complex II in mucosal epithelial cells.The Journal of experimental medicine · 2023Article
- Mucosal-associated invariant T cells have therapeutic potential against ocular autoimmunity.Mucosal immunology · 2022Article
- A Novel Tree Shrew Model of Chronic Experimental Autoimmune Uveitis and Its Disruptive Application.Frontiers in immunology · 2022Article
- Interleukin-22 Influences the Th1/Th17 Axis.Frontiers in immunology · 2021Review
- Lower serum interleukin-22 and interleukin-35 levels are associated with disease status in neuromyelitis optica spectrum disorders.CNS neuroscience & therapeutics · 2020Article
- Interleukin 22 ameliorates neuropathology and protects from central nervous system autoimmunity.Journal of autoimmunity · 2019Article
- Cytokines in uveitis.Current opinion in ophthalmology · 2018Review
- Regulation of IL-22BP in psoriasis.Scientific reports · 2018Article
- Anti-IL-22 Antibody Attenuates Acute Graft-versus-Host Disease via Increasing Foxp3Journal of immunology research · 2018Article
- Immune Privilege and Eye-Derived T-Regulatory Cells.Journal of immunology research · 2018Review
- The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation.PloS one · 2017Article
- The Role of Interleukin-22 and Its Receptor in the Development and Pathogenesis of Experimental Autoimmune Uveitis.PloS one · 2016Article
- AAV-IL-22 modifies liver chemokine activity and ameliorates portal inflammation in murine autoimmune cholangitis.Journal of autoimmunity · 2016Article
- Dental follicle mesenchymal stem cell administration ameliorates muscle weakness in MuSK-immunized mice.Journal of neuroinflammation · 2015Article
- The role of Th17-associated cytokines in the pathogenesis of experimental autoimmune uveitis (EAU).Cytokine · 2015Article
- The multiple sclerosis risk gene IL22RA2 contributes to a more severe murine autoimmune neuroinflammation.Genes and immunity · 2014Article
- Long-term therapeutic effects of mesenchymal stem cells compared to dexamethasone on recurrent experimental autoimmune uveitis of rats.Investigative ophthalmology & visual science · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously reported that IL-17(+) interphotoreceptor retinoid-binding protein (IRBP) 161-180-specific T cells have a strong pathogenic effect in experimental autoimmune uveitis (EAU) induced in B10RIII mice; however, this pathogenic activity is not solely attributable to the major cytokine, IL-17, produced by these cells. To determine whether other cytokines produced by Th17 cells show a stronger association with their pathogenic activity, we studied the role of IL-22 in EAU. IL-22 is one of the major cytokines produced by these cells. Our results showed that administration of small doses of IL-22 to EAU-susceptible mice significantly reduced the severity of EAU. In addition, mice treated with IL-22 generated decreased numbers of IFN-γ(+) and IL-17(+) uveitogenic T cells, but increased numbers of Foxp3(+) regulatory T cells. Mechanistic studies showed that the effect of the injected IL-22 was on CD11b(+) APCs, which expressed increased levels of IL-22R during induction of disease following immunization with uveitogenic Ag. In vitro IL-22 treatment of CD11b(+) APCs collected from Ag-primed mice resulted in increased expression of programmed death ligand-1 and the production of increased amounts of IL-10 and TGF-β. Moreover, IL-22-treated CD11b(+) APCs caused IRBP161-180-specific T cells to lose their uveitogenic activity and acquire immunosuppressive activity, which suppressed the induction of EAU by additional pathogenic IRBP161-180-specific effector T cells.
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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.