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

T he 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 E 2 (PGE 2 ) 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 PGE 2 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 PGE 2 . J Periodontol 1994;65:336–341 .