The role of adhesion molecules and cytokine in periodontitis

牙周炎是由病理性细菌激活的免疫活性细胞引起的慢性炎症。我们研究了辅助分子CD2在NK细胞和T细胞活化中的功能作用。1.蛋白酪氨酸激酶p72^<syk>和磷脂酰肌醇3-激酶参与cd2介导的颗粒胞吐。(1) CD2交联以酪氨酸激酶和PI-3激酶依赖的方式诱导颗粒胞吐。(2) CD2交联诱导Syk的酪氨酸磷酸化并激活其激酶活性。(3) CD2交联诱导转接头蛋白Shc的酪氨酸磷酸化，增强与酪氨酸磷酸化转接头蛋白相关的pi3激酶活性。2.T细胞与CD2的共刺激增强了TCR/ cd3介导的蛋白-酪氨酸激酶p72^<syk>的激活，导致蛋白适配器、Shc和Cbl的酪氨酸磷酸化增加。(1) CD2与CD3的共刺激增强了Syk的酪氨酸磷酸化及其激酶活性。(2) CD2与CD3的共刺激增强了转接蛋白、Shc和Cbl的酪氨酸磷酸化。(3) CD2和CD3共刺激可促进IL-2的产生，显著增强T细胞的增殖。这些结果表明CD2是NK细胞的激活受体，也是T细胞的主要共刺激分子。因此，辅助分子可能通过细胞间和细胞与细胞外基质的相互作用参与炎症过程。

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.