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

点击翻译按钮获取中文摘要

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.