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| This article is part of the supplement: 15th Paediatric Rheumatology European Society (PreS) Congress . Poster presentationCD39: a regulatory role in childhood arthritisInstitute of Child Health, UCL, London, UK
from 15th Paediatric Rheumatology European Society (PreS) Congress Pediatric Rheumatology 2008, 6(Suppl 1):P10doi:10.1186/1546-0096-6-S1-P10 The electronic version of this abstract is the complete one and can be found online at: http://www.ped-rheum.com/content/6/S1/P10
© 2008 Moncrieffe et al; licensee BioMed Central Ltd. BackgroundHuman regulatory T cells (T reg) are classically defined as CD4+ CD25hi Foxp3+. There is increasing evidence that T cells may be subject to regulation via the conversion of proinflammatory ATP to anti-inflammatory adenosine. Methotrexate, the standard therapy for children with JIA, is proposed to work via this mechanism. CD39 belongs to a family of ectoenzymes that convert ATP into an adenosine precursor. ATPase activity may therefore represent an important regulatory mechanism in JIA. Materials and methodsMononuclear cells from peripheral blood (PBMC) and synovial fluid (SFMC) of patients with JIA were analysed in parallel with PBMC from healthy controls. Samples were analysed by 5-colour flow cytometry for expression of Foxp3, CD25 and CD39. FACS sorted cells were assayed for ATPase activity. ResultsCD39 expression was demonstrated on a variety of mononuclear cells in both controls and JIA patients. Increased expression of CD39 was seen on SFMC. Mononuclear cells expressing CD39 showed rapid ATPase activity in vitro. We characterise a proportion of CD39+ T cells with a memory phenotype, express Foxp3 and have regulatory function. ConclusionATPase activity may represent a novel mechanism by which regulation may occur in JIA. CD39+ CD4 cells are enriched in the joint in JIA. CD4+ T cells which express both CD39 and Foxp3 may represent a population with the capability to regulate via multiple mechanisms and therefore be more potent suppressors. Have something to say? Post a comment on this article! |




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