2011 Fiscal Year Final Research Report
Research into the pathophysiology and new therapy of prurigo
| Project/Area Number |
22890054
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
UGAJIN Tsukasa 東京医科歯科大学, 大学院・医歯学総合研究科, メディカルフェロー (40581327)
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| Project Period (FY) |
2010 – 2011
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| Keywords | アトピー性皮膚炎 / 痒疹 / 好塩基球 |
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| Research Abstract |
Basophil play a pivotal role in the pathophysiology of mouse model for prurigo. Zinc-mediated molecule X regulates mediator release from mouse basophil via activation of signaling pathway A. In human basophil, the expression of Zinc-mediated molecule X is strongly, positively correlated with its mediator, indicating that Zinc-mediated molecule X regulates mediator release from basophil not only in mouse but also in human. These data suggest that basophil, activated by Zinc-mediated molecule X, involved in the pathophysiology of prurigo.
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