| Project/Area Number |
22791093
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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 |
Dermatology
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
IMAI Yasutomo 兵庫医科大学, 医学部, 助教 (10529514)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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)
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| Keywords | インターロイキン33(IL-33) / 接触過敏反応 / アレルギー / インターロイキン33 / ケラチノサイト / 皮膚炎 / サイトカイン / ブタクサ / 炎症性皮膚疾患 / インターロイキン18 / IL-1ファミリー |
|---|
| Research Abstract |
IL-33 has been cloned recently as the ligand of ST2. As with IL-1β or IL-18, IL-33 is a member of the IL-1 cytokine family. Effect of IL-33 is dependent on ST2 binding, and its signal is transduced via MyD88, as with IL-1β or IL-18. We examined the role of IL-33 in an immediate type contact hypersensitivity of skin by challenging BALB/c mice with DNFB repeatedly. Wild-type BALB/c mice or ST2-deficient mice were sensitized on shaved back skin with DNFB, and repeatedly challenged with DNFB on the left ear once a week. The ear thickness was measured before and after each challenge. The reactions were hapten specific. Wild-type BALB/c mice showed both immediate and delayed-type reactions, whereas ST2 KO mice did not show any immediate reaction. These results suggest that IL-33 may have an important role in the mechanism of immediate contact hypersensitivity.
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