biostudies-arrayexpressUnknownTranscriptomicsGenomicsProteomicsReuben Noy ScottIllumina HiSeq 4000RNA-seq of coding RNAMus musculusMus musculushttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-16739Joint pathology in rheumatoid arthritis is broadly classified as fibroblast-rich, myeloid-rich, or lymphoid-rich synovitis. How these pathotypes evolve is unknown. Based on the clinical efficacy of biological medicines and targeted inhibitors, we hypothesise that cytokines instruct this process, affecting the rate of onset, severity, and course of disease. These include cytokine signals that define the organisation and maintenance of lymphocyte sentinels in lymphoid-rich synovitis, and others that guide a pauci-immune pathology involving activated stromal cells in fibroblast-rich synovitis. With a long-standing interest in the IL-6 cytokine family, we have identified distinct roles for Jak-STAT signalling in shaping synovitis heterogeneity. Establishing new mouse models that mimic fibroblast-rich, myeloid-rich, and lymphoid-rich synovitis in humans, we propose that wild-type (WT), Il6ra-/-, and Il27ra-/- mice with AIA share hallmarks of these pathotypes. The reported RNA-seq now profiles the transcriptional profile of synovitis in WT, Il6ra-/-, and Il27ra-/- mice with AIA and provides datasets captured at day-3 and day-10 AIA reflecting early and established disease.biostudies-arrayexpressSequencing - Libraries were prepared using the TrueSeq Stranded Total RNA library Prep kit (Illumina) or RNA-seq kit v2 (Life Technologies; 4475936) and sequenced on an Illumina HiSeq 4000 platformNucleic Acid Extraction - RNA was extracted utilising QIAshredders (Qiagen) and RNeasy Mini Kits (Qiagen). On-column DNase digestion (Qiagen) was utilised to remove contaminating genomic DNA.Library Construction - Single-stranded cDNA was synthesized, processed and labelled sequentially using the Ambion® WT (Whole Transcript) Expression Kit, the Affymetrix® Genechip® Poly-A RNA Control Kit and the Terminal Labelling kit.Sample Collection - Studies of antigen-induced arthritis (AIA) were conducted under UK Home Office approvals (PPL-30/1820; PPL-30/2928; PB3E4EE13; PF34A3DC8; PE8BCF782). Mice were challenged (s.c.) with methylated BSA (mBSA; 1 mg/ml emulsified in Complete Freund’s Adjuvant) and 160 ng Bordetella pertussis toxin (i.p.). Following an antigen boost with mBSA and CFA (s.c.), inflammatory arthritis was established by intra-articular (i.a.) administration of mBSA (10μl; 10 mg/ml) into the right knee joint. Synovial tissues were harvested on days 0, 3, and 10 of AIA. Total RNA was isolated from tissue extracts using RNeasy Mini kits (QIAGEN). Libraries were generated from 2-4mg of mRNA following removal of cytoplasmic, mitochondrial, and ribosomal RNA (ribominus transcriptome isolation kit; Ambion). Libraries were prepared using the TrueSeq Stranded Total RNA library Prep kit (Illumina) or RNA-seq kit v2 (Life Technologies; 4475936) and sequenced on an Illumina HiSeq 4000 platform.OrganizationMINSEQE ScoreAssays and DataMAGE-TAB FilesReuben Noy ScottSimon JonesRobert AndrewsGareth JonesfalseBulk RNA-seq of synovial tissues from mice with Antigen Induced Arthritis (AIA) showing distinct hallmarks of synovitis heterogeneityJoint pathology in rheumatoid arthritis is broadly classified as fibroblast-rich, myeloid-rich, or lymphoid-rich synovitis. How these pathotypes evolve is unknown. Based on the clinical efficacy of biological medicines and targeted inhibitors, we hypothesise that cytokines instruct this process, affecting the rate of onset, severity, and course of disease. These include cytokine signals that define the organisation and maintenance of lymphocyte sentinels in lymphoid-rich synovitis, and others that guide a pauci-immune pathology involving activated stromal cells in fibroblast-rich synovitis. With a long-standing interest in the IL-6 cytokine family, we have identified distinct roles for Jak-STAT signalling in shaping synovitis heterogeneity. Establishing new mouse models that mimic fibroblast-rich, myeloid-rich, and lymphoid-rich synovitis in humans, we propose that wild-type (WT), Il6ra-/-, and Il27ra-/- mice with AIA share hallmarks of these pathotypes. The reported RNA-seq now profiles the transcriptional profile of synovitis in WT, Il6ra-/-, and Il27ra-/- mice with AIA and provides datasets captured at day-3 and day-10 AIA reflecting early and established disease.2026-03-26T00:00:00Z2026-03-26T02:03:18.424Z2026-03-11T20:54:15.134ZE-MTAB-16739ERP190597EFO_0002944EFO_0004170EFO_0005518EFO_0003738EFO_0004184