Regulatory mechanisms of mucosal immunity by the ASK family signals
Project/Area Number |
18209055
|
Research Category |
Grant-in-Aid for Scientific Research (A)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Functional basic dentistry
|
Research Institution | The University of Tokyo |
Principal Investigator |
ICHIJO Hidenori The University of Tokyo, Graduate School of Pharmaceutical Sciences, Professor (00242206)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥49,790,000 (Direct Cost: ¥38,300,000、Indirect Cost: ¥11,490,000)
Fiscal Year 2007: ¥24,050,000 (Direct Cost: ¥18,500,000、Indirect Cost: ¥5,550,000)
Fiscal Year 2006: ¥25,740,000 (Direct Cost: ¥19,800,000、Indirect Cost: ¥5,940,000)
|
Keywords | ASK1 / Innate Immunity / Map kinase / Apoptosis / ASK family |
Research Abstract |
Oral cavity functions as the front defense line against pathogens such as bacteria and viruses. Reduced functions of oral mucosa directly leads to the pathogenesis of not only oral diseases but also various systemic diseases including infection. We have recently identified that ASK1, an important component of stress signaling, plays critical roles in innate immunity. We therefore extended our study to explore the potential roles of ASK family signaling molecules in the regulation of mucosal immunity in the present study In this year, we found by using the newly generated in-house monoclonal antibodies to ASK family members that expression of ASK1 was induced by the injury of oral palate. We also found that ASK1 was relatively highly expressed in the cell lines derived from intestinal epidermal tissues compared with other tissues. These results suggested that ASK family members may play important roles in oral mucosal immunity. Moreover, by using the ASK family knock-out mice, we found that ASK family signals play important roles in DSS-induced colitis.
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Report
(3 results)
Research Products
(126 results)