| Budget Amount *help |
¥563,940,000 (Direct Cost: ¥433,800,000、Indirect Cost: ¥130,140,000)
Fiscal Year 2019: ¥87,100,000 (Direct Cost: ¥67,000,000、Indirect Cost: ¥20,100,000)
Fiscal Year 2018: ¥92,300,000 (Direct Cost: ¥71,000,000、Indirect Cost: ¥21,300,000)
Fiscal Year 2017: ¥107,640,000 (Direct Cost: ¥82,800,000、Indirect Cost: ¥24,840,000)
Fiscal Year 2016: ¥111,540,000 (Direct Cost: ¥85,800,000、Indirect Cost: ¥25,740,000)
Fiscal Year 2015: ¥165,360,000 (Direct Cost: ¥127,200,000、Indirect Cost: ¥38,160,000)
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| Outline of Final Research Achievements |
We try to understand the biological and mechanical features in innate immunity using the knockout mice model. We focused on two new research fields: “mRNA stability mechanism” and “disease-specific macrophage subset”. We have showed that phosphorylation of endonuclease Regnase-1 upon inflammatory stimuli is essential for the mRNA stabilization of several inflammation-associated genes. We have also found that Regnase-1 controls colon epithelial regeneration through the mRNA degradation of genes associated with mTOR signaling pathway and purine metabolism. We discovered the new macrophage subset, named SatM, which were critical for the development of fibrosis. Differentiation of SatM cells was governed by CEBP/β expression and these cells were derived from the different progenitor of conventional macrophage lineage. This finding may be possible to develop novel, more specific therapeutic targets with fewer side effects. In addition, we found that the interferon-induced transcription factor Batf2 has an antitumor effect through the TLR7-induced IL-12 production in tumor-associated macrophages, implicating that Batf2 may be an important target in antitumor treatment.
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