tailieunhanh - Báo cáo y học: "Gene expression induced by interleukin-17 in fibroblast-like synoviocytes of patients with rheumatoid arthritis: upregulation of hyaluronan-binding protein TSG-6"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Gene expression induced by interleukin-17 in fibroblast-like synoviocytes of patients with rheumatoid arthritis: upregulation of hyaluronan-binding protein TSG-6 | Arthritis Research Therapy Vol 5 No 4 Kehlen et al. Research article Open Access Gene expression induced by interleukin-17 in fibroblast-like synoviocytes of patients with rheumatoid arthritis upregulation of hyaluronan-binding protein TSG-6 Astrid Kehlen Annette Pachnio Katja Thiele and Jurgen Langner Institute of Medical Immunology Martin Luther University Halle Germany Corresponding author Astrid Kehlen e-mail Received 30 Jul 2002 Revisions requested 12 Sep 2002 Revisions received 19 Mar 2003 Accepted 21 Mar 2003 Published 28 Apr 2003 Arthritis Res Ther 2003 5 R186-R192 DOI ar762 2003 Kehlen et al. licensee BioMed Central Ltd Print ISSN 1478-6354 Online ISSN 1478-6362 . This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Interleukin-17 IL-17 has been characterized as a proinflammatory cytokine produced by CD4 CD45RO memory T cells. Overproduction of IL-17 was detected in the synovium of patients with rheumatoid arthritis RA compared with patients with osteoarthritis. This study examines differentially expressed genes after the stimulation of fibroblastlike synoviocytes of RA patients by IL-17. Among these genes we identified the following tumor necrosis factor-stimulated gene-6 TSG-6 IL-6 IL-8 GRO-p and bone morphogenetic protein-6 with an expression that in the unstimulated control. IL-17 augmented the expression of TSG-6 a hyaluronan-binding protein in a time- and dosedependent manner. IL-17 showed additive effects with IL-1p and tumour necrosis factor-a on the expression of TSG-6 IL-6 and IL-8. The mitogen-activated protein kinase p38 seems to be necessary for the regulation of TSG-6 expression by IL-17 as shown by inhibition with SB203580. Our results support the hypothesis that IL-17 is important in the pathogenesis of RA contributing to an .