| Experiment Id | GSE287676 | Name | mTORC1 promotes adipose tissue ILC2 homeostasis through upregulation of PPAR |
| Experiment Type | RNA-Seq | Study Type | WT vs. Mutant |
| Source | GEO | Curation Date | 2026-08-26 |
| description | 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 PPAR, 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-PPAR axis as a potential therapeutic target for obesity-related metabolic diseases. To investigate the molecular mechanisms underlying the impaired ILC2 function,we conditional knock out rptor gene to delete mTORC1 signaling in adipose tissue ILC2s,we generated Il5RFP-cre (R5/+) Rptorf/f mice to specifically delete mTORC1 signaling in ILC2s (designated as R5/+ Rptorf/f mice for knockout [KO] and R5/+ for wildtype [WT]),then to explore the function of mTORC1 signaling in ILC2s from the mice. |
