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• W2918622557 abstract "Career situation of first and presenting author Post-doctoral fellow. Introduction Juvenile idiopathic arthritis (JIA) is a chronic inflammatory disease (CID) of unknown origin and is characterized by joint inflammation in children and young adults.1 Evidence suggests a strong contribution of memory T cells to disease pathogenicity in JIA. While few markers for T cells adapted to chronic inflammation have been identified.2 3 a comprehensive analysis of what distinguishes pathogenic memory T cells in inflamed tissues of chronic inflammation from protective, circulating memory T cells is still lacking. Objectives To characterize the transcriptional profiles of memory T cells that putatively maintain chronic inflammation in JIA patients. To identify biomarkers that are associated with autoantigen-specific clonotypes among memory T cells in JIA. Methods Memory T cells were isolated from the synovial fluid (SF) and the peripheral blood (PB) of oligoarticular JIA patients and purified by fluorescence-activated cell sorting (FACS). Subsequently, single cell sequencing including T cell receptor (TCR) sequencing was performed on ∼18.000 memory T cells of each JIA patient. Results Memory T cell populations both from the blood and from the SF are heterogenous populations according to their transcriptional expression patterns. The SF harbored a larger population of enriched T memory cell clonotypes than the blood. In addition, enriched memory T helper cell clones in the SF showed a transcriptional pattern of activation compared to non-enriched clonotypes. Finally, small subpopulations of enriched memory T helper cell clones in the SF show a transcriptional signature that resembles transcriptomes obtained by bulk sequencing. Thus, a rather small subpopulation of antigen-specific cells might be responsible for the overall transcriptional character of T cells found at the inflamed sites of CIDs. Conclusions Single cell sequencing combined with TCR sequencing is a powerful tool to identify and characterize subsets of T memory cells in chronic inflammation. The obtained data might be useful to better understand how T cell subsets contribute to disease pathogenicity in CIDs and reveals putative targets that could be therapeutically exploited in order to selectively deplete pathogenic memory T cells. References Prakken B, et al. Juvenile idiopathic arthritis. Lancet 2011. Niesner U, et al. Autoregulation of Th1-mediated inflammation by twist1. J Exp Med 2008. Maschmeyer P, et al. Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo. J Autoimmun 2018. Acknowledgements This work is supported by the European Regional Development Fund (ERDF 2014–2020 and EFRE 1.8/11). Disclosure of Interest None declared." @default.
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• W2918622557 date "2019-03-01" @default.
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• W2918622557 title "P030 Transcriptional landscapes of memory T cells from patients with juvenile idiopathic arthritis" @default.
• W2918622557 doi "https://doi.org/10.1136/annrheumdis-2018-ewrr2019.22" @default.
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