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POS0496 CHILDREN WITH JUVENILE IDIOPATHIC ARTHRITIS HAVE ALTERATIONS IN B AND T FOLLICULAR CELL SUBSETS IN PERIPHERAL BLOOD

Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease in children1. Our group has recently demonstrated that extended oligoarticular (eoJIA) and polyarticular JIA (pJIA) mostly evolve to a rheumatoid arthritis (RA) like phenotype in adulthood2. Disturbances in B cells, T follicular helper (Tfh) and T follicular regulatory (Tfr) cell immune responses are associated with the pathogenesis of RA3,4, but their exact role in JIA development is not entirely known.The main goal of this study was to characterize the frequency and phenotype of B, Tfh and Tfr cells in peripheral blood of children with eoJIA and pJIA when compared to healthy controls and children with persistent oligoarticular JIA (poJIA).Blood samples were collected from children with eoJIA (n=5), pJIA (n=11) and poJIA (n=19) treated with disease modifying anti-rheumatic drugs. A group of age-matched healthy individuals (n=8) was used as control. Peripheral blood mononuclear cells were isolated and the frequency and phenotype of B, Tfh and Tfr cells were evaluated by flow cytometry.The frequency of B, Tfh and Tfr cells was similar between JIA patients and controls. Children with eoJIA and pJIA, but not poJIA, had higher levels of naïve B cells and lower frequencies of post-switch memory B cells and plasmablasts when compared to controls. Th17-like Tfh cells were significantly increased in all JIA patients when compared to controls. B cell phenotype was similar between JIA patients and controls, but a reduced activated phenotype of Tfh cells was observed in JIA patients in comparison to controls.Changes in B and Tfh cell subpopulations, but not in Tfr cells, were found in peripheral blood of children with JIA when compared to controls. The increased frequencies of Th17-like Tfh cells detected in JIA when compared to controls suggests a potential role of these cells in JIA pathogenesis. A treatment effect on the activation state of B, Tfh and Tfr cells cannot be excluded.[1]Ravelli, A. & Martini, A. Juvenile Idiopathic Arthritis. Lancet 369, 767–778 (2007).[2]Oliveira-ramos, F. et al. Juvenile idiopathic arthritis in adulthood: fulfillment of classification criteria for adult rheumatic diseases, long-term outcomes and predictors of inactive disease, functional status and damage. 1–10 (2016)[3]Moura, R. A., Graca, L. & Fonseca, J. E. To B or not to B the conductor of rheumatoid arthritis orchestra. Clin. Rev. Allergy Immunol. 43, 281–291 (2012).[4]Deng, J., Wei, Y., Fonseca, V. R., Graca, L. & Yu, D. T follicular helper cells and T follicular regulatory cells in rheumatic diseases. Nat. Rev. Rheumatol. 15, 475–490 (2019).C. Tomé was supported by a fellowship from Fundação para a Ciência e a Tecnologia (FCT) (PD/BD/135520/2018), Portugal. This work was supported by a grant from Sociedade Portuguesa de Reumatologia.None declared.