Analysis of periodontitis lesions focusing on a new T-cell subset, Th17.
| Project/Area Number |
21792116
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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 |
Periodontal dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
OKUI Takafumi Niigata University, 医歯学系, 特任助教 (10509540)
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| Research Collaborator |
HONDA Tomoyuki 新潟大学, 医歯学系, 特任助教
ITO Harue 新潟大学, 医歯学系, 助教
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 歯周免疫機能学 / Th17 / Treg / IL-17 / FOXP3 / サブセット転換 / CD4^+T細胞ライン / フローサイトメトリー / 免疫組織学的解析 / 制御性T細胞 / RANKL |
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| Research Abstract |
The proportion of IL-17^+ cells (Th17) was higher whereas that of FOXP3^+ regulatory T cells was lower in gingival CD4^+ T-cell lines compared to peripheral blood T-cell lines. The ratio of IL-17^+ FOXP3^+ cells to total FOXP3^+ cells was higher in gingival T-cell lines. Immunohistochemical analysis revealed that the number of IL-17^+ cells and IL-17^+ FOXP3^+ cells was higher in connective tissue area on pocket epithelial side compared to oral epithelial side. These data suggest that Th17 cells accelerate disease progression; furthermore, a part of FOXP3^+ regulatory T cells may convert to the Th17 phenotype sustaining chronic inflammation in periodontitis lesions.
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Report
(3 results)
Research Products
(7 results)
