| Project/Area Number |
25893051
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2013-08-30 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 自然免疫 / マクロファージ / 好中球 / 細胞接着 / 自己免疫疾患 / IRAK / caspase / NF-kB / マクロファージ活性化 / IRAK-M / Caspase |
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| Outline of Final Research Achievements |
The innate immune system plays an important role in host defense and maintenance of homeostasis of the body, and its failure has been shown to cause immune-inflammatory disease. Recently, we further elucidated the newly discovered mechanism of innate immune activation due to cell-cell adhesion between neutrophils and macrophages. The NF-kB activation by cleavage of macrophage inhibitory factor IRAK-M due to caspase6 activation is important in this pathway. We clarified chemokine production, such as RANTES and MIP1α via cell-cell adhesion in addition to inflammatory cytokines such as TNFα. In the future, the further analysis of the molecular mechanisms and their biological significance of this innate immune activation mechanism are expected to contribute to the elucidation of immune-inflammatory disease.
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