{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He Z"],"funding":["NIAMS NIH HHS"],"pagination":["eadt7214"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12767604"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(817)"],"pubmed_abstract":["Rheumatoid arthritis (RA) is preceded by an at-risk stage of disease that can be marked by the presence of anticitrullinated protein antibodies (ACPAs) but the absence of clinically apparent synovitis (clinical RA). Preemptive intervention in at-risk individuals could prevent or delay future tissue damage; however, the immunobiology of this stage is unclear. Using integrative multiomics, we longitudinally profiled at-risk individuals, where one-third of participants developed clinical RA on study. We found evidence of systemic inflammation and signatures of activation in naïve T and B cells of at-risk individuals. During progression to clinical RA, proinflammatory skewing of atypical B cells and expansion of memory CD4 T cells with signatures of activation and B cell help were present with"],"journal":["Science translational medicine"],"pubmed_title":["Progression to rheumatoid arthritis in at-risk individuals is defined by systemic inflammation and by T and B cell dysregulation."],"pmcid":["PMC12767604"],"funding_grant_id":["P30 AR079369"],"pubmed_authors":["Zhang F","Asamoah AG","Mettey RR","Zaim SR","Peng T","Graybuck LT","Reading J","Li XJ","Swanson EG","Parthasarathy V","Garber J","Ochoa A","Collora CE","Genge PC","Kuan EL","Feser ML","Boyle DL","Wang W","Venkatesan P","Firestein GS","Gillespie MA","Roll CR","Okada LY","Krishnan U","Heubeck AT","Fleischer CL","Li R","Goldrath AW","Westermann A","LaFrance CM","Tsaltskan V","Savage AK","Takada H","He Z","Hattel BC","Holers VM","Becker LA","Buckner JH","Gong Q","Stuckey TJ","Ravisankar P","He YD","Speake C","Thai T","Striebich CC","Torgerson TR","Pedrick C","Demoruelle MK","Pebworth MP","Barzideh S","Gustafson CE","Hernandez V","Kuhn KA","Trieu N","Seifert JA","Skene PJ","Deane KD","Siedschlag MD","Musgrove B","Thomson ZJ","Arishi NA","Weiss MDA","Bennett CE","Bumol TF","Dornisch EM","Lazaro L","Tran NTT","Bemis EA","Glass MC","Lord C","Moss L","Ferrannini AC","Kawelo EK","Lee KJ","Criley MAL","Phalen CG","Nguyen KH"],"additional_accession":[]},"is_claimable":false,"name":"Progression to rheumatoid arthritis in at-risk individuals is defined by systemic inflammation and by T and B cell dysregulation.","description":"Rheumatoid arthritis (RA) is preceded by an at-risk stage of disease that can be marked by the presence of anticitrullinated protein antibodies (ACPAs) but the absence of clinically apparent synovitis (clinical RA). Preemptive intervention in at-risk individuals could prevent or delay future tissue damage; however, the immunobiology of this stage is unclear. Using integrative multiomics, we longitudinally profiled at-risk individuals, where one-third of participants developed clinical RA on study. We found evidence of systemic inflammation and signatures of activation in naïve T and B cells of at-risk individuals. During progression to clinical RA, proinflammatory skewing of atypical B cells and expansion of memory CD4 T cells with signatures of activation and B cell help were present with","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-06T11:15:18.442Z","creation":"2026-05-29T03:12:30.704Z"},"accession":"S-EPMC12767604","cross_references":{"pubmed":["40991726"],"doi":["10.1126/scitranslmed.adt7214"]}}