{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Csv":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320067/suppl/GSE320067_norm_data_GEO-20260216.csv.gz","ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320067/suppl/GSE320067_raw_data_GEO-20260216.csv.gz"],"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320067/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE320067"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Type I Interferon Reprograms Intestinal Epithelial Cells for Sustained HIV-1 Latency in CD4+ T Cells of People with HIV-1 Receiving Antiretroviral Therapy","description":"The intestinal environment sustains a state of HIV latency via yet unclear mechanisms. We recently demonstrated that specific cytokines act on intestinal epithelial cells (IEC) to promote viral reservoir (VR) latency or reactivation, with TNF-activated IEC limiting HIV outgrowth in CD4+ T cells of people with HIV (PWH) on antiretroviral therapy (ART). The pro-latency effect of TNF coincided with the induction of IL-32, a pro-inflammatory cytokine overexpressed in ART-treated PWH. Since type I IFNs are strong modulators of IL-32, we investigated IFN-β ability to modulate the crosstalk between IEC and CD4+ T cells via IL-32-dependent mechanisms.","dates":{"publication":"2026/06/18"},"accession":"GSE320067","cross_references":{"GSM":["GSM9533370","GSM9533374","GSM9533373","GSM9533372","GSM9533371","GSM9533378","GSM9533367","GSM9533377","GSM9533366","GSM9533376","GSM9533365","GSM9533364","GSM9533375","GSM9533369","GSM9533368","GSM9533379"],"GPL":["24676"],"GSE":["320067"],"taxon":["Homo sapiens"],"PMID":["[42273706]"]}}