{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE252nnn/GSE252737/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE252737"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"IL-4 Exploits TNF signaling to Shape Its Signature Gene Expression in Human Monocytes. [ChIP-Seq]","description":"Investigation of crosstalk between antagonistic pro- and anti-inflammatory cytokines has focused on mechanisms and functional consequences of cross-inhibition. We investigated cross-regulation between proinflammatory TNF and anti-inflammatory IL-4 in primary human monocytes and in a skin wound-healing model. Surprisingly, TNF functioned mainly as a costimulator of IL-4-induced gene expression, whereas IL-4 selectively inhibited the TNF-induced IFN response, leaving inflammatory gene expression mostly intact. TNF and IL-4 synergistically induced gene sets important for regulating inflammation and tissue repair, which were highly induced during the phase of wound healing when these cytokines are co-expressed. Crosstalk between TNF and IL-4 was mediated by epigenetic chromatin-mediated mechanisms associated with cooperation between NF-κB and STAT6 transcription factors, erasure of negative histone mark H3K27me3, and selective inhibition of IRF1. These results identify a long-sought mechanism for expansion of the IL-4 response, and highlight the complexity of crosstalk between antagonistic cytokines that includes cooperation for select gene responses important in immune response and tissue repair.","dates":{"publication":"2026/09/03"},"accession":"GSE252737","cross_references":{"GSM":["GSM8006072","GSM8006073","GSM8006074","GSM8006075","GSM8006070","GSM8006071","GSM8006117","GSM8006118","GSM8006119","GSM8006113","GSM8006114","GSM8006115","GSM8006116","GSM8006076","GSM8006110","GSM8006077","GSM8006078","GSM8006111","GSM8006112","GSM8006079","GSM8006083","GSM8006084","GSM8006085","GSM8006086","GSM8006080","GSM8006081","GSM8006082","GSM8006128","GSM8006129","GSM8006124","GSM8006125","GSM8006126","GSM8006127","GSM8006087","GSM8006120","GSM8006121","GSM8006088","GSM8006089","GSM8006122","GSM8006123","GSM8006050","GSM8006051","GSM8006052","GSM8006053","GSM8006058","GSM8006059","GSM8006054","GSM8006055","GSM8006056","GSM8006057","GSM8006061","GSM8006062","GSM8006063","GSM8006064","GSM8006060","GSM8006106","GSM8006107","GSM8006108","GSM8006109","GSM8006069","GSM8006102","GSM8006103","GSM8006104","GSM8006105","GSM8006065","GSM8006066","GSM8006067","GSM8006100","GSM8006101","GSM8006068","GSM8006030","GSM8006031","GSM8006036","GSM8006037","GSM8006038","GSM8006039","GSM8006032","GSM8006033","GSM8006034","GSM8006035","GSM8006040","GSM8006041","GSM8006042","GSM8006047","GSM8006048","GSM8006049","GSM8006043","GSM8006044","GSM8006045","GSM8006046","GSM8006094","GSM8006095","GSM8006096","GSM8006130","GSM8006097","GSM8006090","GSM8006091","GSM8006092","GSM8006093","GSM8006139","GSM8006135","GSM8006136","GSM8006137","GSM8006138","GSM8006098","GSM8006131","GSM8006132","GSM8006099","GSM8006133","GSM8006134","GSM8006140","GSM8006141","GSM8006029","GSM8006025","GSM8006026","GSM8006027","GSM8006028","GSM8006021","GSM8006142","GSM8006143","GSM8006022","GSM8006144","GSM8006023","GSM8006024"],"GPL":["16791","18573","24676"],"GSE":["252737"],"taxon":["Homo sapiens"]}}