{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE303nnn/GSE303494/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE303494"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Increased constitutive interferon-β levels and altered CD4 T cell homeostasis induced by expression of a viral glycoprotein","description":"Besides the strong type I interferon (IFN-I) response induced by infections, IFN-I is also produced constitutively at lower levels. Constitutive IFN-I production is often regulated by resident microbiota and is essential for induction of efficient immune responses. Here, we demonstrate in transgenic (tg) mice that expression of a single viral envelope gene, the glycoprotein (GP) of lymphocytic choriomeningitis virus (LCMV), increased constitutive IFN-β levels and induced numerous IFN-stimulated genes (ISGs). In addition, self-antigen-driven CD44highCD62Llow memory-phenotype and regulatory CD4 T cell populations were enlarged in these LCMV GP-tg mice but bona fide antigen-specific memory CD4 T cells were unchanged. In conclusion, our study shows that increased constitutive IFN-β levels induced by expression of a single viral envelope gene and accompanied by upregulated ISGs significantly altered CD4 T cell homeostasis. Furthermore, our data imply that a pathway capable of upregulating constitutive IFN-β levels can sense LCMV GP expression in vivo.","dates":{"publication":"2026/04/02"},"accession":"GSE303494","cross_references":{"GSM":["GSM9128069","GSM9128072","GSM9128073","GSM9128074","GSM9128070","GSM9128071"],"GPL":["24247"],"GSE":["303494"],"taxon":["Mus musculus"],"PMID":["[41972454]"]}}