NDLI: Oral administration of retinoic acid receptor-alpha/beta-specific ligand Am80 suppresses experimental autoimmune uveoretinitis.

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Oral administration of retinoic acid receptor-alpha/beta-specific ligand Am80 suppresses experimental autoimmune uveoretinitis.

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Oral administration of retinoic acid receptor-alpha/beta-specific ligand Am80 suppresses experimental autoimmune uveoretinitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Okada, Annabelle A. Sato, Yasuhiko Keino, Hiroshi Watanabe, Takayo
Description	Country affiliation: Japan Author Affiliation: Keino H ( Department of Ophthalmology, Kyorin University School of Medicine, Tokyo, Japan. keino@eye-center.org)
Abstract	PURPOSE: To determine whether synthetic retinoic acid receptor (RAR)- /ß-specific agonist Am80 reduces inflammation in experimental autoimmune uveoretinitis (EAU). METHODS: Naive CD4(+) T cells were activated with anti-CD3, anti-CD28, and transforming growth factor (TGF)-ß, in the presence or absence of Am80. Intracellular expression of forkhead box p3 (Foxp3) and interleukin (IL)-17 in the activated CD4(+) T cells was assessed by flow cytometry. For induction of EAU, C57BL/6 mice were immunized with human interphotoreceptor retinoid binding protein (IRBP) peptide 1 to 20 (IRBP(1-20)). Am80 was administered orally every other day (3 mg/kg/time point) from day 0 to day 21. In vivo primed draining lymph node cells from vehicle-treated or Am80-treated mice were stimulated with IRBP(1-20), and culture supernatant was harvested for assay of interferon (IFN)-Î³, IL-6, IL-10, and IL-17. The expression of Foxp3 and IL-6 receptor in CD4(+) T cells of draining lymph node cells was assessed by a flow cytometer. RESULTS: Am80 synergized with TGF-ß to induce Foxp3(+) T regulatory cells (Treg) and reciprocally inhibited development of IL-17-producing T helper cells (Th17) induced by TGF-ß and IL-6. Am80 treatment reduced the severity of EAU clinically, and IFN-Î³ and IL-17 production was significantly reduced in Am80-treated mice. In addition, the expression of IL-6 receptor on CD4(+) T cells was downregulated in Am80-treated mice. CONCLUSIONS: These findings demonstrate that Am80 treatment ameliorates severity of EAU and reduces the Th1/Th17 responses. The synthetic retinoid Am80 appears to be a promising agent for preventing autoimmune uveoretinal inflammation.
ISSN	01460404
e-ISSN	15525783
Journal	Investigative Opthalmology & Visual Science
Issue Number	3
Volume Number	52
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2011-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoimmune Diseases Drug Therapy Benzoates Administration & Dosage Disease Models, Animal Receptors, Retinoic Acid Agonists Retinitis Tetrahydronaphthalenes Uveitis Administration, Oral Animals Genetics Immunology Cd4-positive T-lymphocytes Eye Proteins Flow Cytometry Forkhead Transcription Factors Metabolism Gene Expression Interleukin-17 Ligands Lymph Nodes Lymphocyte Activation Mice Mice, Inbred C57bl Nucleic Acid Hybridization Oligonucleotide Array Sequence Analysis Receptors, Interleukin-6 Retinol-binding Proteins Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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