| Project/Area Number |
21591436
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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 | Kochi University |
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Principal Investigator |
SANO Shigetoshi 高知大学, 教育研究部・医療学系, 教授 (80273621)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAJIMA Kimiko 高知大学, 教育研究部・医療学系, 講師 (20403892)
YAMAMOTO Mayuko 高知大学, 教育研究部・医療学系, 助教 (20423478)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 皮膚病理学 / 乾癬 / 表皮セラミド / IL-17 / IL-23 / 表皮バリア / Th17 / γδT細胞 / アトピー性皮膚炎 / TSLP / 表皮バリア破綻 / Th2 |
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| Research Abstract |
Here, we generated Sptlc2 targeted mice under control of the keratin 5 promoter(referred to as K5-SPT-KO mice), by which their keratinocytes were devoid of SPT. These mice demonstrated lower water-holding capacity and barrier dysfunction. From 2 weeks of age, they developed skin inflammation, showing psoriasis-like histopathologic changes. K5-SPT-KO mice showed increased numbers ofγδ-T cells that produced IL-17(γδ-17) in the skin lesion and lymph nodes and most of them also produced IL-22, similar to Th17 cells. In vivo administration of anti-IL-12/ 23p40 antibody ameliorated the skin lesions and reducedγδ-17 cells in K5-SPT-KO mice. Therefore, we conclude that ceramide deficiency in the epidermis results in the development of psoriasis-like lesions.
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