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. 2019 Sep 20;78(12):1712–1721. doi: 10.1136/annrheumdis-2019-216059

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© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

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Transcriptomic divergence in disease-centric pathways that persist despite therapy. Genes enriched (p<0.05, fold difference >1.5) in patients with JIA (n=6 relapse or n=6 remission) that were persistent from prior to after therapy withdrawal, as compared with healthy individuals, were exported to David for functional gene-set enrichment, and gene associations were constructed with Cytoscape using the Reactome database. Five major pathways were dysregulated in relapse and remission patients with JIA compared with healthy controls: (A) TCR activation, (B) TNFα signalling, (C) NF-κB signalling, (D) apoptosis, (E) MAPK signalling (yellow=relapse/remission, blue=remission only). Genes enriched in remission individuals include 1, Fyn; 2, TRAF1; 3, TNFRSF9; 4, CASP1; and 5, IKBKE. MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-kappa B; TCR, T-cell receptor; TNFα, tumour necrosis factor alpha.