| Project/Area Number |
26830058
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory animal science
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
TANG CE 東京理科大学, 研究推進機構生命医科学研究所, 助教 (00572166)
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| Research Collaborator |
IWAKURA Yoichiro
KAKUTA Shigeru
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | C型レクチン / 腸内細菌叢 / サイトカイン / 遺伝子欠損マウス / Ｃ型レクチン |
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| Outline of Final Research Achievements |
The most remarkable achievement in this scientific research is that we found that a member belonging to innate immune C-type lectin receptor family is involved in the regulation of special commensal bacterial population and further influence the development of intestinal inflammation. As the C-type lectin receptor family member, Dectin-1 has been known as the receptor recognizing fungal cell wall component, beta-glucan. In this study, we found that mice deficient with Dectin-1 gene showed drastic suppression of colitis compared with wild-type mice, and this inhibition of intestinal inflammation was caused by over-expansion of commensal Lactobacillus-induced inflammation-suppressing T cells. Treating the mice with Dectin-1-blocade ligand dramatically ameliorated colitis, and these results were published on Cell Host & Microbe (Tang C. et al. 2015;18:183-97) followed by reporting news in Japan. This study suggests a totally new strategy for IBD therapy by targeting on Dectin-1 signaling.
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