Production of interleukin-1 receptor antagonist by human articular chondrocytes 英文参考文献.docVIP
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Production of interleukin-1 receptor antagonist by human articular chondrocytes 英文参考文献
Available online /content/4/3/226
Research article
Production of interleukin-1 receptor antagonist by human
articular chondrocytes
Gaby Palmer1, Pierre-Andre Guerne1, Francoise Mezin1, Michel Maret1, Jerome Guicheux1,3,
Mary B Goldring2 and Cem Gabay1
1Division of Rheumatology, University Hospital, Geneva, Switzerland
2New England Baptist Bone and Joint Institute and Rheumatology Division, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine,
Boston, Massachussetts, USA
3Present address: INSERM EM 9903, School of Dental Surgery, Nantes, France
Correspondence: Cem Gabay, MD, Division of Rheumatology, University Hospital, 26 avenue de Beau-Sejour, 1211 Geneva 14, Switzerland.
Tel: +41 22 382 3501; fax: +41 22 382 3509; e-mail: Cem.Gabay@hcuge.ch
Received: 25 October 2001
Arthritis Res 2002, 4:226-231
Revisions requested: 27 November 2001
Revisions received: 20 February 2002
Accepted: 11 March 2002
This article may contain supplementary data which can only be found
online at /content/4/3/226
? 2002 Palmer et al., licensee BioMed Central Ltd
Published: 8 April 2002
(Print ISSN 1465-9905; Online ISSN 1465-9913)
Abstract
Interleukin-1 receptor antagonist (IL-1Ra) is a natural IL-1 inhibitor possessing anti-inflammatory
properties. IL-1Ra is produced as different isoforms, one secreted (sIL-1Ra) and three intracellular
(icIL-1Ra1, icIL-1Ra2 and icIL-1Ra3), derived from the same gene. We examined the production of
IL-1Ra species by cultured human articular chondrocytes in response to various cytokines. The levels
of IL-1Ra were undetectable in culture supernatants of untreated cells, but were significantly
increased by IL-1β. Cell lysates contained very low levels of IL-1Ra, even in response to IL-1β,
suggesting that chondrocytes produce predominantly sIL-1Ra. IL-6, which had no effect on its own,
enhanced the effect of IL-1β, while dexamethasone prevented the response. We observed by
RT-PCR that
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