<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/GSE329nnn/GSE329046/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Other</omics_type><species>Mus musculus</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329046</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 [TCR-Seq]</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>2026/06/01</publication></dates><accession>GSE329046</accession><cross_references><GSM>GSM9696296</GSM><GSM>GSM9696294</GSM><GSM>GSM9696295</GSM><GPL>24247</GPL><GSE>329046</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>