2019 Fiscal Year Final Research Report
Analysis of the role of IL-22 binding protein in the regulatory mechanism for chronic skin inflammation
| Project/Area Number |
17K15732
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Keywords | 免疫寛容 / 自己免疫 |
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| Outline of Final Research Achievements |
Il22ra2－/－ mice exhibited a more severe IMQ-induced psoriatic dermatitis than WT mice. Furthermore, Il22ra2－/－ mice showed enhanced epidermal infiltration of inflammatory leukocytes and higher transcriptional expression of cytokines and chemokines, as well as epithelial inflammation-related molecules, in psoriatic lesions. Although keratinocytes showed increased proliferation and aberrant differentiation upon stimulation with IL-22, IL-22BP entirely inhibited the IL-22 mediated changes in the functionality of keratinocytes. Thus, our findings suggest that IL-22BP has a critical role in the regulation of IL-22 signaling in keratinocytes to prevent chronic inflammatory skin diseases.
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| Free Research Field |
免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
これまでに未知であった皮膚炎症慢性化病態の成立機構におけるIL-22シグナル調節機構の役割および“IL-22BP機能”に着眼した分子基盤を解明した。さらに、非感染性慢性炎症性皮膚免疫疾患の成立における新たな概念の提唱により、当該領域の発展へ貢献した。
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