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Elucidation of new adhesion mechanism between neutrophils and gingival epithelial cells via thrombomodulin

通过血栓调节蛋白阐明中性粒细胞与牙龈上皮细胞之间的新粘附机制

基本信息

批准号：
13672193
负责人：
MATSUYAMA Takashi
金额：
$ 1.98万
依托单位：
Kagoshima University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13672193/
关键词：
Oral epithelial cells Thrombomodulin Lymphocytes Neutrophils Enzymes 接着機構上皮細胞

项目摘要

Released thrombomodulin has been detected in gingival crevicular fluid with periodontitis from periodontal patients. Gingival epithelial cells express thrombomodulin on their cell surface. In the present study, we investigated the influence of epithelial thrombomodulin by neutrophil protease and the immunoresponse of T lymphocytes in peripheral tissue by the difference of cell density. Neutrophil protease, Elastase but not cathepsin G, released thrombomodulin on oral epithelial cells. The effects occurred in the early phase. On the other hand, released thrombomodulin in the early phase was not related with cytotoxicity by elastase.T cell contact density in peripheral tissues is less than that in lymphoid organs or in the blood stream. The lower density of T cells in peripheral tissues raises a question as to whether the responses of solitary T cells in peripheral tissue are maintained in the same manner as T cells which are more consistently in contact with one another. We investigated the significance of cell-cell contact in the maintenance of T cell response related to TCR/CD28 signaling. The loss of the cell-cell contact results in the induction of a state of unresponsiveness of T cells and the tyrosine phosphorylation through ICAM-1 by cell-cell contact CD54 in advance seemed to be necessary to maintain T cell response to CD3/CD28 signaling

牙周炎患者龈沟液中可检测到血栓调节蛋白的释放。牙龈上皮细胞在其细胞表面表达血栓调节蛋白。本研究探讨了中性粒细胞蛋白酶对上皮血栓调节蛋白的影响，以及细胞密度差异对外周组织T淋巴细胞免疫应答的影响。中性蛋白酶、弹性蛋白酶而非组织蛋白酶G在口腔上皮细胞上释放血栓调节蛋白。影响发生在早期阶段。另一方面，在早期阶段释放的血栓调节蛋白与弹性蛋白酶的细胞毒性无关。外周组织中的T细胞接触密度低于淋巴器官或血流中的T细胞接触密度。外周组织中T细胞的密度较低，这提出了一个问题，即外周组织中孤立T细胞的反应是否以与彼此更一致接触的T细胞相同的方式维持。我们研究了细胞-细胞接触在维持与TCR/CD 28信号相关的T细胞应答中的意义。细胞-细胞接触的丧失导致T细胞的无反应性状态的诱导，并且细胞-细胞接触CD 54预先通过ICAM-1的酪氨酸磷酸化似乎是维持T细胞对CD 3/CD 28信号转导的应答所必需的