GEO series

Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity [II]

GSE279338 Mus musculus Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2025/07/15 Platform GPL21103

Summary

Group-2 innate-lymphoid cells (ILC2s) are critical mediators of the type-2 immune responses in multiple lung pathologies. We show that Piezo1, a mechanosensitive ion channel, plays a key role in regulating ILC2 functions by linking mechanical cues to biochemical signaling pathways. Both murine and human ILC2s strongly express Piezo1, and its activation by Yoda1 selectively enhances IL-13 production through calcium influx, which activates the mTOR-S6K pathway. This pathway leads to translational reprogramming, favoring IL-13 translation. Piezo1-deficient in ILC2s impairs this process, reducing IL-13 levels and resulting in attenuated lung inflammation and fibrosis in mouse models of IL-33- or Alternaria alternata-induced airway inflammation and bleomycin-induced fibrosis. These findings position Piezo1 as a critical mediator of ILC2-driven type-2 immune responses and highlight its potential as a therapeutic target for lung diseases characterized by excessive inflammation. This streamlined understanding of Piezo1 function improves focus on its mechanistic role in lung pathology.

Published in

Piezo1-mediated mechanotransduction regulates the translational activity, function and lung pathogenicity of group 2 innate lymphoid cells

Lim M, Park S, Joo YH et al. · Signal transduction and targeted therapy 2025 · PMID 40841361 · doi:10.1038/s41392-025-02350-4

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Also filed as BioProject PRJNA1172114 and SRA study SRP538104. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40841361) ↗

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