mTORC1 promotes adipose tissue ILC2 homeostasis through upregulation of PPARγ

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.