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  • Title: The inhibition of interferon-gamma-induced upregulation of HLA-DR expression on cultured human gingival fibroblasts by interleukin-1 beta or tumor necrosis factor-alpha.
    Author: Takahashi K, Takigawa M, Arai H, Kurihara H, Murayama Y.
    Journal: J Periodontol; 1994 Apr; 65(4):336-41. PubMed ID: 8195978.
    Abstract:
    The purpose of this study was to examine the effect of inflammatory cytokines on IFN-gamma-induced HLA-DR expression on cultured human gingival fibroblasts by flow cytometry. Natural human IFN-gamma, recombinant human interleukin-1 beta (rhIL-1 beta), and rh tumor necrosis factor-alpha (rhTNF-alpha) were used. IFN-gamma-induced upregulation of HLA-DR expression was inhibited by simultaneously adding rhIL-1 beta or rhTNF-alpha (65.9% and 31.4% inhibition, respectively). Both rhIL-1 beta and rhTNF-alpha induced endogenous prostaglandin E2 (PGE2) from gingival fibroblasts, while IFN-gamma did not. The inhibitory effect of rhIL-1 beta or rhTNF-alpha on IFN-gamma-induced upregulation of HLA-DR expression was partially abated in the presence of indomethacin (reductions of 65.9% and 41.7%, respectively). Both rhIL-1 beta- and rhTNF-alpha-induced endogenous PGE2 synthesis were completely inhibited by adding indomethacin (P < 0.001). The addition of exogenous PGE2 inhibited the IFN-gamma-induced HLA-DR expression (P < 0.001). These observations suggest that the MCH class II expression on human gingival fibroblasts are influenced by the cytokine network and indirectly by the cytokine-mediated fibroblast PGE2.
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