{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE294nnn/GSE294211/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE294211"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Macrophage-Mediated IL1beta/IL23 Signaling Regulates gamma delta (gammadelta) T Cell Immunity Against Non-Tuberculous Mycobacteria","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.","dates":{"publication":"2026/04/01"},"accession":"GSE294211","cross_references":{"GSM":["GSM8900421","GSM8900420"],"GPL":["24676"],"GSE":["294211"],"taxon":["Homo sapiens"]}}