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Rheumatology Advance Access published online on February 28, 2003
Rheumatology, doi:10.1093/rheumatology/keg146
Rheumatology © British Society for Rheumatology 2003; all rights reserved
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© 2003 British Society for Rheumatology

Original Papers

Interferon-{gamma} induces expression of interleukin-18 binding protein in fibroblast-like synoviocytes

B. Möller 1*, J. Paulukat 2, M. Nold 2, M. Behrens 3, N. Kukoc-Zivojnov 1, J. P. Kaltwasser 4, J. Pfeilschifter 2, H. Mühl 2

1 Rheumazentrum Rhein-Main/Medizinische Klinik III
2 Pharmazentrum Frankfurt, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany
3 Institut für Kardiovaskuläre Physiologie, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany
4 Rheumazentrum Rhein-Main/Medizinische Klinik III, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany

* Corresponding author. E-mail: b.moeller{at}em.uni-frankfurt.de.

Received 9 November 2001 ; accepted 4 September 2002

Abstract

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)-{gamma} markedly up-regulated IL-18BPa mRNA levels. Induction was accompanied by release of IL-18BPa immunoreactvity from FLS. Conditioned media from IFN-{gamma}-stimulated FLS cultures reduced IL-12/IL-18-dependent IFN-{gamma} production by peripheral blood mononuclear cells.

Conclusion. The present data imply that IFN-{gamma}-activated synoviocytes mediate a negative feedback loop via IL-18BPa, which may limit IL-18 biological activity in arthritis.

Key words: IFN-{gamma}, IL-18BP, Synoviocyte, Fibroblast, Rheumatoid arthritis.
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