## Abstract ## Objective To study the regulation of interleukinβ18 binding protein (ILβ18BP) production by rheumatoid arthritis (RA) or control peripheral blood mononuclear cells (PBMCs) and by RA synovial tissue cells, and to compare the levels of ILβ18BP messenger RNA (mRNA) expression in whole
Detection of interleukin 8 biological activity in synovial fluids from patients with rheumatoid arthritis and production of interleukin 8 mRNA by isolated synovial cells
β Scribed by Fionula M. Brennan; Claus O. C. Zachariae; David Chantry; Christian G. Larsen; Martin Turner; Ravinder N. Maini; Kouji Matsushima; Marc Feldmann
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 462 KB
- Volume
- 20
- Category
- Article
- ISSN
- 0014-2980
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β¦ Synopsis
and Kennedy Institute of Rheumat ology a, London Detection of interleukin 8 biological activity in synovial fluids from patients with rheumatoid arthritis and production of interleukin 8 mRNA by isolated synovial cells*
The presence of neutrophils in the synovial joint of patients with rheumatoid arthritis (RA) is thought to be due to the activity of chemotactic factors released by activated cells in the joint.We have shown in this report, for the first time, the abundance of one such factor, interleukin 8 (IL 8), in the synovial fluid of patients both with RA and other n o n -U joint diseases, and the spontaneous production of IL8 mFWA by RA synovial cells in culture.There was no correlation between the levels of chemotactic activity and IL8 protein, suggesting that other factors with similar neutrophil chemotactic activity are also present in the synovial fluid exudate. In support of this concept neither the level of chemotactic activity nor IL 8 protein levels correlated with neutrophil or leukocyte infiltration, indicating that the mechanism of migration into the inflammatory environment of the joint is complex. Such migration is likely to be due to a number of chemotactic signals in addition to IL8, which may either synergize with, or inhibit, the action of IL 8.
* This work was funded by the Arthritis and Rheumatism Council, Xenova and the Sunley Trust.
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