<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE269nnn/GSE269069/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE269069</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>EV-mediated Monocytes Reprogramming in Mycobacterium tuberculosis Infection</name><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.</description><dates><publication>2026/06/30</publication></dates><accession>GSE269069</accession><cross_references><GSM>GSM8305840</GSM><GSM>GSM8305843</GSM><GSM>GSM8305841</GSM><GSM>GSM8305842</GSM><GPL>30173</GPL><GSE>269069</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>