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.

journal_name

J Periodontol

authors

Takahashi K,Takigawa M,Ami H,Kurihara H,Murayama Y

doi

10.1902/jop.1994.65.4.336

subject

Has Abstract

pub_date

1994-04-01 00:00:00

pages

336-341

issue

4

eissn

0022-3492

issn

1943-3670

journal_volume

65

pub_type

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