The role of adhesion molecules and cytokine in periodontitis

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Periodontitis is chronic inflammation caused by immunocompetent cells activated by pathologic bacteria. We investigated the functional roles of accessory molecule, CD2 on NK and T cell activation. 1.Involvement of protein tyrosine kinase p72^<syk> and phosphatidylinositol 3-kinase in CD2-mediated granular exocytosis in the natural killer cell line. (1) Crosslinking of CD2 induces granular exocytosis in tyrosine kinase and PI-3 kinase dependent fashion. (2) Crosslinking of CD2 induces tyrosine phosphorylation of Syk and activates its kinase activity. (3) Crosslinking of CD2 induces tyrosine phosphorylation of adapter protein, Shc and enhances PI3-kinase activity associated with tyrosine phosphorylated adapter proteins. 2.Costimulation of T cells with CD2 augments TCR/CD3-mediated activation of protein-tyrosine kinase p72^<syk>, resulting in increased tyrosine phosphorylation of adapter of proteins, Shc and Cbl. (1) Costimulation of CD2 with CD3 enhances tyrosine phosphorylation of Syk and its kinase activity. (2) Costimulation of CD2 with CD3 enhances tyrosine phosphorylation of adapter proteins, Shc and Cbl. (3) Costimulation of CD2 with CD3 enhances IL-2 production and markedly augments T cell proliferation. These results indicate that CD2 is an activating receptor in NK cells and a major costimulatory molecules for T cells. Thus, accessory molecules may be involved in inflammatory process through cell to cell and cell to extra cellular matrix interaction.