monocytes are essential for inhibition of synovial t-cell glucocorticoid-mediated apoptosis in rheumatoid arthritis单核细胞是必不可少的对于抑制滑膜t细胞在类风湿性关节炎glucocorticoid-mediated细胞凋亡.pdfVIP

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monocytes are essential for inhibition of synovial t-cell glucocorticoid-mediated apoptosis in rheumatoid arthritis单核细胞是必不可少的对于抑制滑膜t细胞在类风湿性关节炎glucocorticoid-mediated细胞凋亡.pdf

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monocytes are essential for inhibition of synovial t-cell glucocorticoid-mediated apoptosis in rheumatoid arthritis单核细胞是必不可少的对于抑制滑膜t细胞在类风湿性关节炎glucocorticoid-mediated细胞凋亡

Available online /content/10/6/R147 Vol 10 No 6 Open Access Research article Monocytes are essential for inhibition of synovial T-cell glucocorticoid-mediated apoptosis in rheumatoid arthritis Dimitrios Makrygiannakis, Shankar Revu, Petra Neregård, Erik af Klint, Omri Snir, Cecilia Grundtman and Anca Irinel Catrina Department of Rheumatology, Karolinska University Hospital and Karolinska Institutet, Stockholm, S-17176, Sweden Corresponding author: Anca Irinel Catrina, anca.catrina@ki.se Received: 14 Jul 2008 Revisions requested: 21 Aug 2008 Revisions received: 22 Nov 2008 Accepted: 19 Dec 2008 Published: 19 Dec 2008 Arthritis Research Therapy 2008, 10:R147 (doi:10.1186/ar2582) This article is online at: /content/10/6/R147 © 2008 Makrygiannakis et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction Rheumatoid arthritis (RA) is characterized by Results Intra-articular glucocorticoids reduced ST T cells but synovial inflammation with local accumulation of mononuclear not macrophage number. ST apoptosis levels were unchanged cells such as macrophages and lymphocytes. We previously following treatment, virtually absent from lymphoid aggregates, demonstrated that intra-articular glucocorticoids decrease the and minimal in CD3+ cells both before and after treatment. RA synovial tissue (ST) T-cell population and therefore aimed to SF T cells were resistant to glucocorticoid-induced ap