| Project/Area Number |
21791709
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Kyorin University |
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Principal Investigator |
KEINO Hiroshi Kyorin University, 医学部, 講師 (90328211)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | レチノイド受容体 / 自己免疫性ぶどう膜網膜炎 / Th17 / 制御性T細胞 / レチノイン酸 / ぶどう膜炎 |
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| Research Abstract |
Recent studies have demonstrated that retinoids suppress T cell differentiation into Th1 and Th17 cells while promoting the generation of Foxp3^+ T regulatory cells in vitro. We examined whether retinoic acid receptor (RAR) agonist, retinoic acid and RAR-α/β specific agonist Am80 would be effective in experimental autoimmune uveoretinitis (EAU), an animal model that shares many clinical and histological features with human uveitic disorders. Administration of retinoic acid and Am80 was effective in suppressing inflammation in EAU, mainly by suppressing differentiation of Th1/Th17 effector cells. In addition, the expression of IL-6 receptor α on CD4^+ T cells was down-regulated in retinoic acid /Am80-treated mice. Am80 treatment during the effector phase only was capable of delaying inflammation in EAU. Thus, retinoic acid and the synthetic retinoid, Am80 appears to be a promising agent for preventing and treating autoimmune uveoretinal inflammation mediated by the Th1/Th17 pathway.
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