The role of adhesion molecules and cytokines in chronic periodontitis

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Periodontitis is chronic inflammation caused by immunocompetent cells activated by pathologic bacteria. We investigated the interaction between T cells and fibroblasts, and costimulatory effects of CD2 stimulation on IL-2-mediated NK cell proliferation and signal pathways through CD2 and IL-2 using NK cell line, NK3.3.PHA-activated T cells adhered to ICAM-1 and ECMs in a dose-dependent manner and PMA markedly enhanced the adhesion of PHA-activated T cells to ICAM and ECMs. The CC-chemokines, such as MCP-1 and RANTES, enhanced adhesion of PHA-activated T cells to ICAM-1, but not to ECMs, whereas, the CX3C-chemokine, fractalkine had no effect on PHA-activated T cell adhesion. To examine the natural setting of the interaction between T cells and fibroblasts, the binding of PHA-activated T cells to immobilized fibroblast like cell line, E11 cells was examined. We found that adhesion of PHA-activated T cells to E11 cells was ICAM-1 dependent and that MCP-1 and RANTES, but not fractalkine, enhanced binding of PHA-activated T cells to E11 cells. These results suggest that some chemokines have important roles in adhesion of T cells to fibroblasts, which may be involved in pathogenesis of periodontitis through enhancing immunologic reaction at the inflammatory sites.Costimulation of CD2 crosslinking significantly enhanced IL-2-mediated NK3.3 proliferation. Crosslinking of CD2 induced tyrosine phosphorylation of protein tyrosine kinase, Syk and adapter proteins, Shc and Cbl. However, IL-2 stimulation enhanced tyrosine phosphorylation of Shc, but not Syk nor Cbl. Cbl constitutively associates with Grb2 through N-SH3 domain, whereas Shc associates with Grb2 through SH2 domain in an activation-dependent manner.