{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE300nnn/GSE300310/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE300310"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Human Endogenous Retroviruses Drive Type-I Interferon Signaling activation in Early Rheumatoid Arthritis","description":"Substantial reactivation of HERVs was observed in both synovial tissues and PBMCs from early RA patients. Differentially expressed HERVs regulate adjacent ISGs expression by providing cis-regulatory elements. Moreover, excessive cytoplasmic HERVs trigger a type I interferon (IFN-I) response through the dsRNA-RIG-I-IRF3-IFN-I axis. Targeting endogenous retroviruses exhibited potential therapeutic benefits in both CIA mouse models and RA patient-derived ex vivo models. Specifically, the IFN-I inducible HERV.MLT2B2, a novel primate-specific retroelement, acts as a key driver of the antiviral gene IFI44L, establishing a positive feedback loop that amplifies IFN-I signaling.","dates":{"publication":"2026/06/05"},"accession":"GSE300310","cross_references":{"GSM":["GSM9058169","GSM9058158","GSM9058168","GSM9058157","GSM9058159","GSM9058161","GSM9058160","GSM9058163","GSM9058152","GSM9058162","GSM9058165","GSM9058154","GSM9058164","GSM9058153","GSM9058167","GSM9058156","GSM9058166","GSM9058155"],"GPL":["24676"],"GSE":["300310"],"taxon":["Homo sapiens"]}}