| Project/Area Number |
13470443
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
MATSUMOTO Goichi Kanagawa Dental College, Oral Surgery, instructor, 歯学部, 講師 (60199867)
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| Co-Investigator(Kenkyū-buntansha) |
OHMI Yasushi Kanagawa Dental College, Oral Surgery, Assistant, 歯学部, 助手 (10318892)
USHAKU Lee Kanagawa Dental College, Oral Surgery, Assistant, 歯学部, 助手 (90288085)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥9,500,000 (Direct Cost: ¥9,500,000)
Fiscal Year 2002: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2001: ¥6,900,000 (Direct Cost: ¥6,900,000)
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| Keywords | LFA-1 / NKT / costimulation / α-GalCer / DC / DC / CD28 / 樹状細胞 / NKT細胞 |
|---|
| Research Abstract |
Natural killer T (NKT) cells produce large amounts of cytokines associated with both the Th1 response (IFN-γ) and Th2 response (IL-4) after being stimulated by the synthetic CD1d ligand α-galactosylceramide (α-GalCer) by their invariant Vα14 receptor. However, the role played by adhesion or co-stimulation molecules in the activation of NKT cells by α-GalCer remains unclear. To address this issue, LFA-1^+ and CD28^+ mice were used to investigate IL-4 and IFN-γ production by NKT cells following α-GalCer stimulation. LFA-1^+ mice showed increased IL-4 production in response to in vitro and in vivo polarized Th2-type responses, represented by activation of B cells and serum IgE elevation. In contrast, impairment of production of IL-4 and IFN-γ in CD28^+ mice resulted in a profound inability to polarize the Th2-type response, represented by the abolishment of serum IgE. These results imply that the LFA-1 adhesion receptor and the CD28 co-stimulatory receptor selectively regulate Th1- and Th2-like functions of α-GalCer-activated NKT cells.
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