| Project/Area Number |
23689030
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Nara Institute of Science and Technology (2013)
Osaka University (2011-2012) |
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Principal Investigator |
KAWAI Taro 奈良先端科学技術大学院大学, バイオサイエンス研究科, 准教授 (50456935)
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| Research Collaborator |
JIAN Zou 大阪大学, 大学院医学系研究科, 博士課程
SURYA Pandey 大阪大学, 大学院医学系研究科, 博士課程
TAKESHI Kondo 大阪大学, 大学院医学系研究科, 博士課程
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥27,430,000 (Direct Cost: ¥21,100,000、Indirect Cost: ¥6,330,000)
Fiscal Year 2013: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2012: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2011: ¥9,750,000 (Direct Cost: ¥7,500,000、Indirect Cost: ¥2,250,000)
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| Keywords | 自然免疫 / DNAセンサー / シグナル伝達 / インターフェロン / ウイルス / 自己免疫疾患 / ウイルス感染 |
|---|
| Research Abstract |
Upon recognition of double-stranded DNA derived from virus or bacteria by innate immunity, host cells produce type I interferon or other inflammatory mediators essential for host defense. However, mechanisms involved in DNA recognition are unclear. In addition, it is suggested that self-DNA derived from damaged cells are recognized by innate immunity and this is considered to be responsible for development of inflammatory and autoimmune diseases. In this research, we identified MRE11, a protein involved in repair responses, as a candidate protein involved in self-DNA recognition and induction of type I interferon and inflammatory cytokines. MRE11 binds to and colocalizes with immunostimulatory DNA, and cells that do not express MRE11 have defects in induction of these cytokines by immunostimulatory DNA. These findings may shed light on our understanding of pathogenesis of autoimmunity in which aberrant DNA recognition is involved.
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