| Project/Area Number |
20790502
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
KATAKURA Kyoko Fukushima Medical University, 医学部, 助教 (70423788)
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| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 炎症性腸疾患 / Toll-like receptor / 制御性T細胞 / I型IFN / イミキモド / Toll-like receptor(TLR) / サイトメガロウイルス感染 / 樹状細胞 / 自然免疫 |
|---|
| Research Abstract |
We investigated whether TLR7 agonist Imiquimod (IMQ) protects mice from colonic inflammation. And to confirm the induction of regulatory T cells (Tregs) by type-1 IFN from plasmacytoid dedritic cells (pDCs), we generated mouse bone marrow derived pDC and co-cultured with CD4^+T cells isolated from mouse spleen with or without IMQ stimulation. Administration of IMQ significantly suppressed colonic inflammation of TNBS-induced colitis, and we could detect CD4^+CD25^+Foxp3^+Tregs induction in IMQ stimulated co-cultured cells. These results suggest that IMQ protects mice from TNBS colitis through induction of Tregs by type-1 IFN from pDCs. Moreover, IMQ would offer a novel tool for the treatment in inflammatory bowel disease.
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