The Inhibition of Interferon-γ-Induced Upregulation of HLA-DR Expression on Cultured Human Gingival Fibroblasts by Interleukin-1β or Tumor Necrosis Factor-α

Abstract

The purpose of this study was to examine the effect of inflammatory cytokines on IFN-γ-induced HLA-DR expression on cultured human gingival fibroblasts by flow cytometry. Natural human IFN-γ, recombinant human interleukin-1β (rhIL-1β), and rh tumor necrosis factor-α (rhTNF-α) were used. IFN-γ-induced upregulation of HLA-DR expression was inhibited by simultaneously adding rhIL-1β or rhTNF-α (65.9% and 31.4% inhibition, respectively). Both rhIL-1β and rhTNF-α induced endogenous Prostaglandin E₂ (PGE₂ ) from gingival fibroblasts, while IFN-γ did not. The inhibitory effect of rhIL-1β or rhTNF-α on IFN-γ-induced upregulation of HLA-DR expression was partially abated in the presence of indomethacin (reductions of 65.9% and 41.7%, respectively). Both rhIL-1β- and rhTNF-α-induced endogenous PGE₂ synthesis were completely inhibited by adding indomethacin (P < 0.001). The addition of exogenous PGE2 inhibited the IFN-γ-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 . J Periodontol 1994;65:336-341.

Keywords: Cytokines; HLA-DR antigens; fibroblasts; flow cytometry.