| Project/Area Number |
10671695
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
RIKIISHI Hidemi School of Dentistry, Tohoku University, Assistant Prof., 歯学部, 講師 (70091767)
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| Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Shunji School of Dentistry, Tohoku University, Assistant Prof., 歯学部, 助手 (10241639)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Superantigen / Lipopolysaccharide / Apoptosis / CD80 / Periodontal disease / LPS / サイトカイン |
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| Research Abstract |
We demonstrated previously that superantigen (SAg) enhances CD80 expression on human monocytes, whereas treatment with SAg in the presence of lipopolysaccharide (LPS) markedly decreases the percentage of CD80ィイD1+ィエD1 peripheral blood monocytes, indicating that the presence of low levels of CD80 on monocytes inhibits CD27 expression on SAg-activated T cells due to insufficient delivery of positive signals via CD28/CD80 interaction. To assess the role of LPS in this inhibition, the relationship between SAg-dependent apoptosis and regulation of CD80 expression of CD14ィイD1+ィエD1 monocytes was examines. SAg enhanced the annexin V-positive or PI-positive (propidium iodide) levels in monocytes, whereas LPS-treated monocytes were resistant to the apoptotic action of SAg. This SAg-induced killing was abrogated by antagonists anti-CD95 (Fas) and anti-CD95 ligand monoclonal antibodies, suggesting a CD95-based pathway of apoptosis. Furthermore, apoptosis of monocytes, preferentially CD80ィイD1-ィエD1 monocytes, was affected by high-level expression of CD95 by SAg, and the survival required down-regulation of CD95 expression by LPS over the SAg action. During these culture periods, the number of CD80ィイD1+ィエD1 monocytes was nearly constant. These observations strongly suggested that a small fraction of CD80ィイD1+ィエD1 monocytes is selectively resistant to CD95-based apoptosis, and the percentage of CD80ィイD1+ィエD1 monocytes increases through escape from SAg-induced preferential apoptosis, which is inhibited by addition of LPS.
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