Function of cell adhesion molecules and cytokine in the periodontal disease.

T细胞克隆跨越ifn - γ内皮细胞（EC）屏障的体外研究在Aa和抗原呈递细胞（APC）的刺激下，转运能力明显增强。其他刺激（Con A,IL-2）不促进转运。阻断APC提供的第二个信号（CTLA4-Ig）可显著减少转运。此外，用单克隆抗体阻断Th1或Th2克隆上的粘附分子LFA-1导致75-97%的转运受阻。ifn - γ治疗EC可导致II类MHC表达显著上调，提示EC可呈递抗原。ifn - γ显著增加Th1克隆的迁移。IL-4抑制Th1的迁移，增强Th2的迁移。移行抗原特异性T淋巴细胞的能量可以作为一种保护机制，限制Th1细胞对细菌抗原的广泛增殖，并由此产生潜在破坏性的ifn - γ和IL-2。转运能也可能通过限制自身反应性牙龈T细胞的增殖，在外周T细胞耐受中发挥作用。第二项研究的目的是研究环氧化酶-1 （COX-1）和环氧化酶-2 （COX-2）在促炎细胞因子白介素-1 β (il -1 β)刺激下人牙周韧带（PDL）成纤维细胞产生前列腺素（PG）的作用，并研究白细胞介素-4 (IL-4)（一种Th2细胞因子）和干扰素-g (ifn - γ)（一种Th1细胞因子）对细胞产生PG的影响。本研究提示，il -1 β刺激的人PDL细胞产生PEG_2与COX-2有关，IL-4和ifn - γ通过抑制COX-2的表达而下调PEG_2的产生，而对COX-2的表达没有影响。我们也获得了一些关于ALP基因的结果。

T cell clones across an IFN-gamma endothelial cell (EC) barrier in vitro. Transmigration was greatly enhanced after stimulation by Aa and antigen presenting cells (APC). Other stimuli (Con A,IL-2) did not enhance transmigration. Blocking of a second signal provided by APC (with CTLA4-Ig) significantly reduced transmigration. Also, blocking of the adhesion melecule LFA-1 on Th1 or Th2 clones with monoclonal antibody resulted in 75-97% obstruction of transmigration. IFN-gamma treatment of EC resulted in dramatic upregulation of class II MHC expression suggesting that EC could present antigen. IFN-gamma significantly increased Th1 clone transmigration. IL-4 decreased Th1 trasmigration, but enhanced Th2 transmigration. Anergy of transmigrated antigen-specific T lymphocytes can be a protective mechanism that limits extensive Th1 cell proliferation to bacterial antigens and the resultant production of potentially destructive IFN-gamma and IL-2. Transmigration anergy may also play a role in peripheral Tcell tolerance by limiting proliferation of autoreactive gingival T cells. The purpose of the second study was to investigate the involvement of cyclooxygease-1 (COX-1) and cyclooxygenase-2 (COX-2) in prostaglandin (PG) production by human periodontal ligament (PDL) fibroblasts stimulated with a proinflammatory cytokine, interleukin-1beta (IL-1beta), and to examine the effect of interleukin-4 (IL-4), a Th2 cytokine, and interferon-g (IFN-gamma)、a Th1 cytokine, on PG production by the cells. This study suggests that COX-2 are responsible for PEG_2 production by IL-1beta-stimulated human PDL cells and that IL-4 anmd IFN-gamma down-regulate PEG_2 production through inhibition of COX-2 expression and with no effect on COX-2 expression. We also have obtained several results as to ALP gene.