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The etiological significance of superantigen in periodontal disease and its possible role

超抗原在牙周病中的病因学意义及其可能的作用

基本信息

批准号：
10671695
负责人：
RIKIISHI Hidemi
金额：
$ 1.98万
依托单位：
TOHOKU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671695/
关键词：
Superantigen Lipopolysaccharide Apoptosis CD80 Periodontal disease LPS サイトカイン

项目摘要

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.

我们先前证明超抗原（SAg）增强人单核细胞上的CD 80表达，而在脂多糖（LPS）存在下用SAg处理显著降低外周血单核细胞上的CD 80 β D1+ CD 80 β D1的百分比，表明单核细胞上低水平的CD 80的存在抑制了SAg活化的T细胞上的CD 27表达，这是由于通过CD 28/CD 80的阳性信号传递不足。CD 80相互作用。为了评估LPS在这种抑制中的作用，检测了SAg依赖性细胞凋亡与CD 14 β D1+ CD 80 D1单核细胞表达调节之间的关系。SAg增强了单核细胞中膜联蛋白V阳性或PI阳性（碘化丙啶）的水平，而LPS处理的单核细胞对SAg的凋亡作用具有抗性。这种SAg诱导的杀伤被拮抗剂抗CD 95（Fas）和抗CD 95配体单克隆抗体废除，表明基于CD 95的凋亡途径。此外，单核细胞的凋亡，优先CD 80 CD 95 D1-CD 80 D1单核细胞，受SAg的高水平表达的CD 95的影响，和生存需要下调CD 95的表达由LPS超过SAg的行动。在这些培养期间，CD 80 β D1+ CD 80 β D1单核细胞的数量几乎恒定。这些观察结果强烈表明，一小部分CD 80 β D1+ CD 80 D1单核细胞选择性地抵抗基于CD 95的凋亡，并且CD 80 β D1+ CD 80 D1单核细胞的百分比通过逃避SAg诱导的优先凋亡而增加，这被添加LPS抑制。