2012 Fiscal Year Final Research Report
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 |
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| Research Field |
Ophthalmology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Keywords | 眼免疫学 / ぶどう膜炎 / ベーチェット病 / T細胞 |
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| 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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Research Products
(4 results)
