Receptor activator NFκB ligand (RANKL) expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathy, osteoarthritis, and from normal patients: semiquantitative and quantitative analysis

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dc.contributor.authorCrotti, T.
dc.contributor.authorSmith, M.
dc.contributor.authorWeedon, H.
dc.contributor.authorAhern, M.
dc.contributor.authorFindlay, D.
dc.contributor.authorKraan, M.
dc.contributor.authorTak, P.
dc.contributor.authorHaynes, D.
dc.date.issued2002
dc.description.abstractObjectives: To compare receptor activator of NF-kB ligand (RANKL) production in the synovial tissue from patients with active rheumatoid arthritis (RA), inactive RA, spondyloarthropathies (SpA), osteoarthritis, and from normal subjects. In addition, to establish the cell lineages expressing RANKL in these tissues. Methods: Immunohistological analysis of frozen synovial tissue biopsy specimens was performed using a monoclonal antibody (mAb) to detect RANKL. Sections were evaluated by computer assisted image analysis and semiquantitative analysis to compare RANKL expression between groups. Dual and sequential labelling with mAb RANKL and cell lineage specific monoclonal antibodies were used to determine the types of cells expressing RANKL. Results: Higher levels of RANKL were expressed in tissues from patients with active RA and SpA than in tissues from patients with inactive RA, osteoarthritis, and from normal subjects. RANKL protein was associated with CD3 antigen-positive lymphocytes and some macrophages. RANKL was predominantly associated with activated, memory T cells (CD45Ro positive cells) in patients with active RA and spondyloarthropathy (SpA). Conclusions: The highest levels of RANKL were detected in patients with RA with active synovitis and in some patients with SpA. An increase in RANKL in the inflamed joint of patients with RA, produced by infiltrating activated T cells and macrophages, is likely to be an important cause of joint erosions in RA.
dc.description.statementofresponsibilityT N Crotti, M D Smith, H Weedon, M J Ahern, D M Findlay, M Kraan, P P Tak and D R Haynes
dc.identifier.citationAnnals of the Rheumatic Diseases, 2002; 61(12):1047-1054
dc.identifier.doi10.1136/ard.61.12.1047
dc.identifier.issn0003-4967
dc.identifier.issn1468-2060
dc.identifier.orcidCrotti, T. [0000-0002-5422-3758]
dc.identifier.urihttp://hdl.handle.net/2440/6635
dc.language.isoen
dc.publisherBritish Med Journal Publ Group
dc.rights© 2002 by Annals of the Rheumatic Diseases
dc.source.urihttp://ard.bmj.com/cgi/content/abstract/61/12/1047
dc.subjectbone
dc.subjectrheumatoid arthritis
dc.subjectreceptor activator NF-B ligand
dc.subjectimmunohistochemistry
dc.subjectspondyloarthropathies
dc.titleReceptor activator NFκB ligand (RANKL) expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathy, osteoarthritis, and from normal patients: semiquantitative and quantitative analysis
dc.title.alternativeReceptor activator NFkappaB ligand (RANKL) expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathy, osteoarthritis, and from normal patients: semiquantitative and quantitative analysis
dc.typeJournal article
pubs.publication-statusPublished

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