Th2 profile abrogates cutaneous barrier function. -New insight in the pathogenesis of atopic dermatitis-
| Project/Area Number |
20591323
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Oita University |
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Principal Investigator |
HATANO Yutaka Oita University, 医学部, 講師 (80336263)
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| Co-Investigator(Kenkyū-buntansha) |
KATAGIRI Kazumoto 獨協医科大学, 越谷病院, 教授 (00204420)
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| Project Period (FY) |
2008 – 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: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | Th2サイトカイン / 皮膚バリア機能 / アトピー性皮膚炎 / コルネオデスモゾーム / デスモグレイン1 / PPARα |
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| Research Abstract |
1. Th2 cytokines inhibit the permeability barrier recovery via reduction of formation and secretion of lamellar bodies.
2. Th2 cytokines abrogate integrity of stratum corneum via reduction of density of corneodesmosomes, which results from inhibitory effects of Th2 cytokines on expression of desmoglein 1.
3. Th2 cytokines reduce the expression of PPARα in epidermis, resulting in barrier abnormality in atopic dermatitis.
These results suggest that Th2 cytokines are involved in making atopic dermatitis refractory and that activation of PPARα might be one of the new therapeutic targets in atopic dermatiris.
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Report
(4 results)
Research Products
(3 results)
