GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320067/suppl/GSE320067_norm_data_GEO-20260216.csv.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320067/suppl/GSE320067_raw_data_GEO-20260216.csv.gzftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE320nnn/GSE320067/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE320067GEOGSEfalseType I Interferon Reprograms Intestinal Epithelial Cells for Sustained HIV-1 Latency in CD4+ T Cells of People with HIV-1 Receiving Antiretroviral TherapyThe 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.2026/06/18GSE320067GSM9533370GSM9533374GSM9533373GSM9533372GSM9533371GSM9533378GSM9533367GSM9533377GSM9533366GSM9533376GSM9533365GSM9533364GSM9533375GSM9533369GSM9533368GSM953337924676320067Homo sapiens[42273706]