2015 Fiscal Year Final Research Report
Analysis of host defense mechanism against dermatomycosis via IL-17A/F induced by C-type lectin
| Project/Area Number |
26860867
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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 |
Dermatology
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| Research Institution | Chiba University |
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Principal Investigator |
IWASAWA Mari 千葉大学, 医学部附属病院, 助教 (70375723)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 皮膚科学 / 真菌症 |
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| Outline of Final Research Achievements |
IL-17 reportedly played a key role in mouse systemic candidiasis in C-type lectin dependent way. However, defense mechanisms to epicutaneous infection of C. albicans, termed epicutaneous candidiasis (ECC) remain unclear. Here, we developed ECC mouse model, in which C. albicans was inoculated occlusively on shaved skin for 7 days. In this model, skin inflammation reached a peak on day 2 with neutrophil infiltration and abated by day 7 in WT, while Il17aｆ-/- mice showed inflamed skin even on day 7 with high fungal burden, showing the importance of IL-17 for ECC defense. When analyzed in Clec7aClec4n-/-, Tlr2-/-, Myd88-/-, Fcer1g-/- and Card9-/- mice, none of these receptors or molecules was involved in ECC, suggesting unknown mechanisms of C. albicans recognition, contrary to the systemic infection. In conclusion, IL-17 plays a pivotal role in host defense to ECC.
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| Free Research Field |
皮膚科学
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