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Macrophage-Mediated IL1beta/IL23 Signaling Regulates gamma delta (gammadelta) T Cell Immunity Against Non-Tuberculous Mycobacteria [scRNA-seq]

GSE290965 Mus musculus Expression profiling by high throughput sequencing 3 samples Submitted 2026/03/01 Platform GPL24247
Summary
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.
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Also filed as BioProject PRJNA1229835 and SRA study SRP566997. Searching any of these in the dataset finder brings you back here.

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