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Real-time quantitative PCR used as a biomarker for synovial gene expression after oral prednisolone therapy in patients with rheumatoid arthritis

Arthritis Research & Therapy
Springer (Biomed Central Ltd.)
Publication Date
DOI: 10.1186/ar1682
  • Poster Presentation
  • Biology
  • Medicine


S1 Available online Speaker abstracts S1 Stem cells now and in the future in medicine A Smith MRC Centre Development in Stem Cell Biology, Institute for Stem Cell Research, University of Edinburgh, UK Arthritis Res Ther 2005, 7(Suppl 1):S1 (DOI 10.1186/ar1506) Abstract not submitted. S2 Chaperonins and the regulation of immunity GS Panayi, VC Corrigall Academic Department of Rheumatology, King’s College London, Guy’s Hospital, London, UK Arthritis Res Ther 2005, 7(Suppl 1):S2 (DOI 10.1186/ar1507) Chaperonins have classically been thought of as intracellular molecules involved in the correct folding of proteins. Their expression is upregulated during times of stress such as heat (hence their common nomenclature as heat shock proteins [HSP]), anoxia, hypoglycaemia and reactive oxygen species [1]. These are condi- tions found in infected tissues or in tissues with chronic inflammation such as the rheumatoid synovium. In their intracellular location they protect the cell from apoptotic death due to stress. Increasingly chaperonins have been recognised to subserve extracellular functions for which they have received the name ‘chaper- okines’ since they bind to specific receptors on the cell surface and activate cells of the innate immune system to secrete inflammatory cytokines, chemokines and small molecular weight mediators such as prostaglandins [2]. Indeed, an early event in inflammation is cell stress/necrosis leading to the release of HSP60 and HSP70 that binds via a CD14-mediated mechanism to Toll-like receptors 2 and 4 [2] as part of the ‘danger’ signal [3]. The secretion of tumour necrosis factor alpha, IL-1, IL-12 and other chemokines prepares the environment for a TH1 adaptive immune response. It is now recognised that some chaperonins, such as BiP and HSP27, may activate the innate immune system to secrete anti-inflamma- tory cytokines, such as IL-10 [4,5] that may skew the adaptive immune response to TH2. Recent work by our group has

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