{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE269nnn/GSE269069/"]},"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=GSE269069"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"EV-mediated Monocytes Reprogramming in Mycobacterium tuberculosis Infection","description":"Extracellular vesicles (EVs) secreted by Mtb-infected macrophages (MΦEVMtb) may influence the host innate immune response to Mtb-infection, but specific EV-induced mechanisms that regulate such cell phenotype changes are not yet known. We report that PMBCs cultured with MΦEVMtb exhibit a marked classical to intermediate monocyte polarization effect, as detected by single-cell RNA sequencing and flow cytometry results. Moreover, this effect appears to correspond with the activation of the alternative NF-κB pathway, and can be partially recapitulated by treating PBMCs with EV derived from recombinant cell line that overexpresses TRAF1, a direct regulator of this pathway. Collectively, we depict an EV-mediated monocyte reprogram landscape in the context of Mtb infection and highlight a potential link between EV and pathogenesis of tuberculosis.","dates":{"publication":"2026/06/30"},"accession":"GSE269069","cross_references":{"GSM":["GSM8305840","GSM8305843","GSM8305841","GSM8305842"],"GPL":["30173"],"GSE":["269069"],"taxon":["Homo sapiens"]}}