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

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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.