<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Reuben Noy Scott</submitter><instrument_platform>Illumina HiSeq 4000</instrument_platform><study_type>ATAC-seq</study_type><organism>Mus musculus</organism><species>Mus musculus</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16747</full_dataset_link><description>Joint 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.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sequencing - Libraries were pooled and sequenced on an Illumina sequencer to generate paired-end 50-base pair reads.</sample_protocol><sample_protocol>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 3 and 10 of AIA. Genomic DNA was isolated from the inflamed synovium of mice with AIA, and from mice before the induction of AIA (taken as control tissues). ATAC-seq was performed using 100,000 nuclei per sample as described in the manufacturer’s instruction protocol (Illumina, FC-121-1030). After amplification, library DNA was isolated (Qiagen MiniElute kit), size selected, and sequenced (Illumina HiSeq4000). All samples were quantified (Qubit; Invitrogen) before sequencing (Illumina HiSeq4000; 40-70M reads/sample).</sample_protocol><sample_protocol>Nucleic Acid Extraction - ATAC-seq libraries were generated from fresh cells using the ATAC-Seq Kit (Active Motif, catalog# 53150).</sample_protocol><sample_protocol>Library Construction - Libraries were quantified using the Qubit dsDNA HS Assay Kit (Thermo Fisher Scientific) and profiled using the D5000 ScreenTape on TapeStation 4200 (Agilent Technologies).</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><pubmed_authors>Reuben Noy Scott</pubmed_authors><pubmed_authors>Simon Jones</pubmed_authors><pubmed_authors>Robert Andrews</pubmed_authors><pubmed_authors>Gareth Jones</pubmed_authors></additional><is_claimable>false</is_claimable><name>ATAC-seq of synovial tissues from mice with Antigen Induced Arthritis (AIA) showing distinct hallmarks of synovitis heterogeneity</name><description>Joint 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.</description><dates><release>2026-03-26T00:00:00Z</release><modification>2026-03-26T02:03:18.435Z</modification><creation>2026-03-11T16:05:35.778Z</creation></dates><accession>E-MTAB-16747</accession><cross_references><ENA>ERP190679</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0007045</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>