OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis

Background Previous studies have demonstrated a plasticity of effector-T-cells regarding CCR6 expression in autoimmune disorders. In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ p...

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Veröffentlicht in:Annals of the rheumatic diseases 2013-06, Vol.71 (Suppl 3), p.72-72
Hauptverfasser: Sustal, K.N., Almanzar, G., Trippen, R., Höfner, K., Prelog, M.
Format: Artikel
Sprache:eng
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Zusammenfassung:Background Previous studies have demonstrated a plasticity of effector-T-cells regarding CCR6 expression in autoimmune disorders. In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ production). Objectives The present study was aimed to investigate the CCR6+ T-cell phenotype and its plasticity in children with Juvenile idiopathic arthritis (JIA). Methods Peripheral blood mononuclear cells (PBMCs) of children with JIA (n=25 in clinical remission on medication; n=10 with disease flare) and age-matched healthy donors (HD) (n=21) were analyzed by flowcytometry to assess the phenotype, cytokine production and proliferation of T-cells expressing the chemokine receptor CCR6+. CCR6+ T-cells were separated via magnetic bead isolation. Results The proportion of CCR6+ T-cells (CD4+ gate) was significantly increased in patients with disease flare (mean 6.3±3.7%) compared to those in remission (3.3±2.7%) or HD (4.0±1.9%) (p
ISSN:0003-4967
1468-2060
DOI:10.1136/annrheumdis-2012-eular.1741