| Project/Area Number |
13854021
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| Research Category |
Grant-in-Aid for Scientific Research (S)
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| Allocation Type | Single-year Grants |
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| Research Field |
病態科学系歯学(含放射線系歯学)
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
AZUMA Miyuki Tokyo Medical and Dental University, Graduate Sch Med and Dent Sciences, Professor, 大学院・医歯学総合研究科, 教授 (90255654)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIGUCHI Masaaki Tokyo Medical and Dental University, Graduate Sch Med and Dent Sciences, Assistant Professor, 大学院・医歯学総合研究科, 助手 (20372443)
小園 裕子 東京医科歯科大学, 歯学部付属病院, 助手 (30197107)
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| Project Period (FY) |
2001 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥108,550,000 (Direct Cost: ¥83,500,000、Indirect Cost: ¥25,050,000)
Fiscal Year 2005: ¥12,350,000 (Direct Cost: ¥9,500,000、Indirect Cost: ¥2,850,000)
Fiscal Year 2004: ¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2003: ¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2002: ¥24,700,000 (Direct Cost: ¥19,000,000、Indirect Cost: ¥5,700,000)
Fiscal Year 2001: ¥34,190,000 (Direct Cost: ¥26,300,000、Indirect Cost: ¥7,890,000)
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| Keywords | Immunology / Dentistry / Infectious diseases / Cancer / Costimulatory molecules / Oral diseases / Dendritic cells / T lymphocytes / 口腔粘膜疾患 / 免疫制御 / 歯髄 / 粘膜上皮細胞 / 免疫 / 歯髄炎 / 骨吸収 / 補助シグナル / 破骨細胞 / 細胞間相互作用 |
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| Research Abstract |
We investigated expression and function of costimulatory molecules including PD-1:B7-H1/B7-DC, ICOS:B7h, BTLA, B7-H3, and B7-H3 in oral immune responses and diseases. B7-H1 that is one of ligands for PD-1 was induced on a various inflammatory tissue cells as well as immune cells, whereas expression of B7-DC was limited on activated dendritic cells (DCs) and macrophages. Our results demonstrate the involvement of PD-1:B7-H1 pathway in immune regulation based on the studies from the comparative analyses between expression and clinical features and prognosis in oral lichen planus (OLP) and oral cancer, and in addition, the in vivo treatments with blocking monoclonal antibodies in models of skin contact hypersensitivity and oral cancer. A ligand of ICOS, B7h was less expressed as compared with B7-H1, but was expressed at high levels on endothelial cells in OLP and oral cancer tissues, suggesting the involvement of B7h in lymphocyte infiltration into the tissues.
We have established a murine
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pulpitis model using fresh-frozen decalcified hard tissue sections and an immunofluorescence staining and examined dental pulp after dentin exposure. We found that two types of DCs, CD11c^+F4/80^- and CD11c^-F4/80^+, exist in dental pulp. CD11c^+F4/80^- cells located in the pulp-dentin border and expressed constitutively TLR2, TLR4, and CD205. CD11c^-F4/80^+ cells located in the central pulp and were lacking the above molecules. Both types of cells migrated rapidly to the P-D border of treated cusp side, but a part of F4/80^+ cells alone induced a costimulatory molecule CD86. Simultaneously, F4/80^+CD86^+ cells in the regional lymph nodes increased, suggesting the migration of these cells from the pulp. These results suggest that antigen-capture and migration of pulpal DCs may occur and the migrated DCs may induce a consequent adoptive immune response. Our findings provide important information for estimating the healing properties of dental pulp and for developing possible treatments of dental restoration. Less
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