Mechanisms of immune suppression for activated T cells by infliximab therapy in patients with Behcet's uveoretinitis.
Project/Area Number |
23791971
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Ophthalmology
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Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
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Project Period (FY) |
2011 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 眼免疫学 / ぶどう膜炎 / ベーチェット病 / T細胞 |
Research Abstract |
Previous studies suggested that the intraocular inflammation in Behcet’s disease (BD) is predominated by Th1 and Th17 immune responses. Recently, Th22 cells were identified as a novel Th lineage associated with autoimmune diseases. We showed that Th22-type T cell clones established from ocular samples from patients with BD produced large amounts ofTh22 associated cytokines IL-22 and TNF-α. CD4+ T cells from PBMCs of BD patients differentiated into Th22 cells. Th22 cells exposed to infliximab, anti-TNF-αantibody, in vitro failed to produce IL-22. Moreover, Th22 cells were isolated from mice with experimental autoimmune uveitis (EAU), an animal model of BD, and intraocular T cells from EAU produced large amounts of IL-22 in the presence of retinal antigens. Theseresults suggest that Th22 cells may play a key role in the ocular inflammation in BD. Suppression of Th22 cells by infliximab may protect uveitis patients with BD from severe ocular inflammation.
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Report
(3 results)
Research Products
(6 results)