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Effects of adhesion molecules and mechanism of gingival fibroblast rescue butyric acid-induced T-cell apoptosis.

粘附分子的作用及牙龈成纤维细胞拯救丁酸诱导的 T 细胞凋亡的机制。

基本信息

批准号：
14571746
负责人：
OCHIAI Kuniyasu
金额：
$ 1.98万
依托单位：
Meikai University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

项目摘要

We have previously demonstrated that human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis via proinflammatory cytokines such as IL-6 and IL-11, which are produced by fibroblasts stimulated with butyric acid. In this study, we determined if T cell adhesion to human gingival fibroblasts influenced the susceptibility of T cells to butyric acid-induced apoptosis. We have shown that the number of Jurkat T cells adherent to gingival fibroblasts (Gin 1 cells) was significantly increased by the addition of butyric acid. All Jurkat cells that adhered to Gin-1 cells remained viable, while the non-adherent Jurkat cells dropped into apoptosis. The increase in T cell adhesion to fibroblasts was also observed when Jurkat cells, but not Gin 1 cells, were pretreated with butyric acid. CD44, very late antigen (VLA)-2 and VLA-5 but not leukocyte function-associated antigen 1 (LFA-1) and VLA-4 expressions on Jurkat cells were increased following treatment with butyric acid. Furthermore, pretreatment of butyric acid-sensitized Jurkat cells with monoclonal antibodies against CD44, VLA-2 and VLA-5, but not LFA-1 and VLA-4, followed by co-culture with Gin-1 cells abrogated T-cell adhesion to fibroblasts. These results indicate that the T-cell adherence to fibroblasts is enhanced by butyric acid, and that butyric acid-induced T-cell apoptosis is down-regulated by T-cell adhesion to gingival fibroblasts through an interaction with the adhesion molecules CD44, VLA-2 and VLA-5 expressed on T cells stimulated with butyric acid.

我们先前已经证明，人牙龈成纤维细胞通过丁酸刺激的成纤维细胞产生的促炎细胞因子如IL-6和IL-11来挽救丁酸诱导的T细胞凋亡。在这项研究中，我们确定了T细胞与人牙龈成纤维细胞的黏附是否影响了T细胞对丁酸诱导的凋亡的敏感性。我们发现丁酸能显著增加Jurkat T细胞与牙周成纤维细胞(Gin-1细胞)的黏附。所有与Gin-1细胞黏附的Jurkat细胞仍然存活，而未黏附的Jurkat细胞陷入凋亡。用丁酸处理Jurkat细胞时，T细胞与成纤维细胞的粘附性增加，而用丁酸处理Gin-1细胞时，T细胞与成纤维细胞的粘附性增加。丁酸作用后Jurkat细胞CD44、VLA-2和VLA-5表达增加，而白细胞功能相关抗原1(LFA-1)和VLA-4表达增加。此外，用抗CD44、VLA-2和VLA-5的单抗(而不是抗LFA-1和VLA-4的单抗)预处理丁酸致敏的Jurkat细胞，然后与Gin-1细胞共培养，可减少T细胞与成纤维细胞的黏附。这些结果表明，丁酸可促进T细胞与成纤维细胞的黏附，并通过与丁酸刺激的T细胞上表达的黏附分子CD44、VLA-2和VLA-5相互作用，下调丁酸诱导的T细胞凋亡。