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mTORC1 promotes adipose tissue ILC2 homeostasis through upregulation of PPARγ

GSE287676 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2026/03/04 Platform GPL34290
Summary
The disruption of adipose tissue group 2 innate lymphoid cells (ILC2s) is associated with obesity-induced insulin resistance. However, the molecular mechanisms underlying the impaired ILC2 function in obesity remain unclear. In this study, we show that obesity-induced lipid accumulation suppresses mechanistic target of rapamycin complex 1 (mTORC1) activity in ILC2s. Deletion of Rptor, a critical adaptor protein in mTORC1, results in reduced numbers of ILC2 and diminished type 2 cytokine production in ILC2s, leading to enhanced adipose tissue inflammation and insulin resistance. Mechanistically, mTORC1 signal facilitates the expression of PPARγ, which promotes mitochondrial biogenesis and ST2 expression to sustain ILC2 metabolic and functional fitness. Together, our data identify mTORC1 as a crucial regulator of adipose tissue ILC2 homeostasis and highlight mTORC1-PPARγ axis as a potential therapeutic target for obesity-related metabolic diseases.
Published in
Obesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling
Hu L, Wang D, Chen Y et al. · Cellular & molecular immunology 2026 · PMID 41593294 · doi:10.1038/s41423-026-01389-9
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Also filed as BioProject PRJNA1214238 and SRA study SRP559119. Searching any of these in the dataset finder brings you back here.

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