<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/GSE294nnn/GSE294211/</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=GSE294211</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Macrophage-Mediated IL1beta/IL23 Signaling Regulates gamma delta (gammadelta) T Cell Immunity Against Non-Tuberculous Mycobacteria</name><description>Mechanistic Insights. Our study reveals the crucial role of gammadelta T cells in non-tuberculous mycobacteria (NTM) infection. We observed a significant increase and activation of gammadelta T cells in mice infected with MAB or with MAB infection combined with pulmonary fibrosis. Depletion of gammadelta T cells worsened the infection, while transfer of gammadelta T cells reversed this effect. Mechanistically, we found that MAB infection stimulates macrophages to produce IL-1beta and IL-23, which promotes the expansion of gammadelta T17 cells. MAB can also directly activate gammadelta T cells, leading to the clearance of MAB through an IL-17A-dependent pathway. Our findings suggest that gammadelta T cells represent a potential therapeutic target for NTM infections.</description><dates><publication>2026/04/01</publication></dates><accession>GSE294211</accession><cross_references><GSM>GSM8900421</GSM><GSM>GSM8900420</GSM><GPL>24676</GPL><GSE>294211</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>