Induction of regulatory T cells by histone modification for the treatment of inflammation bowel disease
| Project/Area Number |
26713026
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Toyama Prefectural University (2015-2016)
Keio University (2014) |
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Principal Investigator |
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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 |
¥23,660,000 (Direct Cost: ¥18,200,000、Indirect Cost: ¥5,460,000)
Fiscal Year 2016: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
Fiscal Year 2015: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
Fiscal Year 2014: ¥9,620,000 (Direct Cost: ¥7,400,000、Indirect Cost: ¥2,220,000)
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| Keywords | 制御性T細胞 / エピジェネティクス / 短鎖脂肪酸 / HDAC / 炎症性腸疾患 / IBD |
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| Outline of Final Research Achievements |
Butyrate has a potential to inhibit class I HDAC isozymes but not class II HDAC isozymes. In time course analysis, butyrate preferentially induce Foxp3, a master regulator of regulatory T cells (Treg), but not other master regulators of Th1, Th2 and Th17 (e.g., T-bet, Gata3, Ror-gamma t). Treg induction by using HDAC isozyme specific inhibitors revealed that the butyrate induce Foxp3 probably through the inhibition of HDAC1 and HDAC3 that belong to class I HDAC.
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Report
(4 results)
Research Products
(9 results)
