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T-cell activation without proliferation in juvenile idiopathic arthritis.

Black AP, Bhayani H, Ryder CA, Gardner-Medwin JM, Southwood TR - Arthritis Res. (2001)

Bottom Line: 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.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.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.

View Article: PubMed Central - PubMed

Affiliation: MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital,Headington, Oxford, UK.

ABSTRACT
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.

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Relation between erythrocyte sedimentation rate and expression of CD71 on T cells from synovial fluid from patients with juvenile idiopathic arthritis. Points represent individual synovial fluid samples. Data show line of linear regression (P = 0.0005). ESR = erythrocyte sedimentation rate; MFI = median fluorescence intensity.
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Figure 4: Relation between erythrocyte sedimentation rate and expression of CD71 on T cells from synovial fluid from patients with juvenile idiopathic arthritis. Points represent individual synovial fluid samples. Data show line of linear regression (P = 0.0005). ESR = erythrocyte sedimentation rate; MFI = median fluorescence intensity.

Mentions: No consistent variation of T-cell activation or differentiation status was observed for most of the clinical parameters (Table 3). There was, however, an association between CD71 expression on SF T cells and the vigour of the acute-phase response as measured by the erythrocyte sedimentation rate (P = 0.0005; Fig. 4).


T-cell activation without proliferation in juvenile idiopathic arthritis.

Black AP, Bhayani H, Ryder CA, Gardner-Medwin JM, Southwood TR - Arthritis Res. (2001)

Relation between erythrocyte sedimentation rate and expression of CD71 on T cells from synovial fluid from patients with juvenile idiopathic arthritis. Points represent individual synovial fluid samples. Data show line of linear regression (P = 0.0005). ESR = erythrocyte sedimentation rate; MFI = median fluorescence intensity.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC111019&req=5

Figure 4: Relation between erythrocyte sedimentation rate and expression of CD71 on T cells from synovial fluid from patients with juvenile idiopathic arthritis. Points represent individual synovial fluid samples. Data show line of linear regression (P = 0.0005). ESR = erythrocyte sedimentation rate; MFI = median fluorescence intensity.
Mentions: No consistent variation of T-cell activation or differentiation status was observed for most of the clinical parameters (Table 3). There was, however, an association between CD71 expression on SF T cells and the vigour of the acute-phase response as measured by the erythrocyte sedimentation rate (P = 0.0005; Fig. 4).

Bottom Line: 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.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.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.

View Article: PubMed Central - PubMed

Affiliation: MRC Human Immunology Unit, Institute of Molecular Medicine, John Radcliffe Hospital,Headington, Oxford, UK.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus