Interferon-γ induces expression of interleukin-18 binding protein in fibroblast-like synoviocytes

B. Möller, J. Paulukat, M. Nold, M. Behrens, N. Kukoc-Zivojnov, J. P. Kaltwasser, J. Pfeilschifter, H. Mühl

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37 Citations (Scopus)


Objective. To investigate expression of the endogenous antagonist of interleukin 18 (IL-18) bioactivity, IL-18 binding protein isoform a (IL-18BPa), in fibroblast-like synoviocytes (FLS). Methods. Long-term cultured FLS from rheumatoid arthritis (RA), osteoarthritis (OA) and spondylarthropathy patients were analysed for spontaneous and cytokine-induced IL-18BPa expression. Messenger RNA and release of IL-18BPa were assessed by semi-quantitative and quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) as well as immunoblot analysis, respectively. Results. All investigated FLS cultures expressed low amounts of IL-18BPa transcripts. However, there was no detectable release of IL-18BPa from unstimulated synoviocytes. Of the investigated cytokines, only interferon (IFN)-γ markedly up-regulated IL-18BPa mRNA levels. Induction was accompanied by release of IL-18BPa immunoreactvity from FLS. Conditioned media from IFN-γ-stimulated FLS cultures reduced IL-12/IL-18-dependent IFN-γ production by peripheral blood mononuclear cells. Conclusion. The present data imply that IFN-γ-activated synoviocytes mediate a negative feedback loop via IL-18BPa, which may limit IL-18 biological activity in arthritis.

Original languageEnglish
Pages (from-to)442-445
Number of pages4
Issue number3
Publication statusPublished - 1 Mar 2003
Externally publishedYes


  • Fibroblast
  • IFN-γ
  • IL-18BP
  • Rheumatoid arthritis
  • Synoviocyte

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