Open Access Open Badges Research article

T-cell activation without proliferation in juvenile idiopathic arthritis

Antony PB Black1, Hansha Bhayani25, Clive AJ Ryder3, Janet MM Gardner-Medwin3 and Taunton R Southwood4*

Author Affiliations

1 MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, UK

2 Formerly of Department of Rheumatology, University of Birmingham

3 Department of Paediatric Rheumatology, Birmingham Children's Hospital-NHS Trust, Birmingham, UK

4 Department of Rheumatology, University of Birmingham, Edgbaston, Birmingham, UK

5 Deceased

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Arthritis Res 2002, 4:177-183  doi:10.1186/ar403

Published: 21 November 2001


A study was done to determine if the differentiation and activation phenotype of T cells in synovial fluid (SF) from patients with juvenile idiopathic arthritis (JIA) is associated with T-cell proliferation in situ. Mononuclear cells were isolated from 44 paired samples of peripheral blood and SF. Differentiation and activation markers were determined on CD4 and CD8 T cells by flow cytometry. Cell-cycle analysis was performed by propidium iodide staining, and surface-marker expression was also assessed after culture of the T cells under conditions similar to those found in the synovial compartment. The majority of the T cells in the SF were CD45RO+CD45RBdull. There was greater expression of the activation markers CD69, HLA-DR, CD25 and CD71 on T cells from SF than on those from peripheral blood. Actively dividing cells accounted for less than 1% of the total T-cell population in SF. The presence or absence of IL-16 in T-cell cultures with SF or in a hypoxic environment did not affect the expression of markers of T-cell activation. T cells from the SF of patients with JIA were highly differentiated and expressed early and late markers of activation with little evidence of in situ proliferation. This observation refines and extends previous reports of the SF T-cell phenotype in JIA and may have important implications for our understanding of chronic inflammation.

activation; chronic inflammation; differentiation; T cells