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The Inhibition of Interferon‐γ‐Induced Upregulation of HLA‐DR Expression on Cultured Human Gingival Fibroblasts by Interleukin‐1β or Tumor Necrosis Factor‐α
Author(s) -
Takahashi Keiso,
Takigawa Masayuki,
Ami Hideo,
Kurihara Hidemi,
Murayama Yoji
Publication year - 1994
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1994.65.4.336
Subject(s) - tumor necrosis factor α , tumor necrosis factor alpha , downregulation and upregulation , interferon γ , interleukin , interferon , interferon gamma , human leukocyte antigen , immunology , cancer research , medicine , interleukin 4 , cytokine , chemistry , antigen , gene , biochemistry
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 .