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TLR2 in γδ T cells is required for metabolic support of IL-17A ocular mucosal immune response to a commensal bacterium [ATAC-seq]

GSE236383 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2024/05/15 Platform GPL21103
Summary
The ocular surface is colonized by commensal microbiota, which tune the local mucosal immune response. However, the mechanisms underlying the induction of an IL-17 response by γδ T cells in response to ocular commensal bacteria, particularly Corynebacterium mastitidis (C. mast), have not been fully investigated. Here, we demonstrated that intrinsic TLR2 activation in γδ T cells by commensal microbiota is required for their IL-17A production and fatty acid oxidation. We also identified IκBζ, a transcription factor whose expression is upregulated by TLR2 signaling, as a key regulator to enhance the expression of genes responsible for IL-17A production and FAO program. This study highlights the role of TLR2-mediated transcriptional regulation in targeting effector cytokines and metabolic programs to support IL-17A responses to commensal bacteria.
Published in
TLR2 Supports γδ T cell IL-17A Response to ocular surface commensals by Metabolic Reprogramming
Zhu W, Xu X, Nagarajan V et al. · bioRxiv : the preprint server for biology 2025 · PMID 38712203 · doi:10.1101/2024.04.01.587519
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Also filed as BioProject PRJNA990734 and SRA study SRP447133. Searching any of these in the dataset finder brings you back here.

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