2015 Fiscal Year Final Research Report
A molecular mechanism of atopic manifestations of hyper-IgE syndrome
| Project/Area Number |
25293232
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Keywords | 原発性免疫不全症 / アトピー性皮膚炎 / STAT3 |
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| Outline of Final Research Achievements |
We identified that hyper-IgE syndrome is caused by dominant negative mutations of the STAT3 gene. Almost all the patients with hyper-IgE syndrome suffer from atopic dermatitis, but a molecular mechanism of the skin manifestation remain unidentified and no treatment other than palliative treatment is available. To address this issue, we establish a model mouse of hyper-IgE syndrome. We evaluated several skin-inflammation models and found that repetitive oxazolone application to the skin is the most useful model for atopic dermatitis by evaluating itching behavior, thickening of epidermis, recruitment of CD4+T cells and eosinophils, increased oxazolone-specific IgE antibody and Th2 cytokines.
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| Free Research Field |
小児科学
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