2016 Fiscal Year Final Research Report
Analysis of the role of S100A8/A9 and its novel receptors in chronic inflammation in atopic dermatitis
Project/Area Number |
26860899
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Dermatology
|
Research Institution | Tokyo Medical University |
Principal Investigator |
YAMAMOTO Mami 東京医科大学, 医学部, 助教 (60421062)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | アトピー性皮膚炎 / S100A8/A9 |
Outline of Final Research Achievements |
Previously, we reported a positive feedback loop between S100A8/A9 and proinflammatory cytokines mediated by extracellular matrix metalloproteinase inducer (EMMPRIN), an S100A9 receptor. Therefore, we assumed that S100A8/A9 plays an important role in the chronic inflammation that arises from barrier disruption in atopic dermatitis. In this study, we identified neuroplastin-β (NPTNβ) as a novel S100A8 receptor. The S100A8-NPTNβ signal activated keratinocyte proliferation, while the S100A9-EMMPRIN signaling pathway induced skin inflammation. NPTNβ and EMMPRIN formed homodimers and a heterodimer. S100A8 and S100A9 were strongly expressed and co-localized with these receptors in the lesional skin of atopic dermatitis. These results indicate that NPTNβ and EMMPRIN form a functional heterodimeric receptor for S100A8/A9 and play a critical role in atopic dermatitis.
|
Free Research Field |
皮膚科学
|