| First Author | Hu L | Year | 2026 |
| Journal | Cell Mol Immunol | Volume | 23 |
| Issue | 3 | Pages | 301-314 |
| PubMed ID | 41593294 | Mgi Jnum | J:380904 |
| Mgi Id | MGI:8292700 | Doi | 10.1038/s41423-026-01389-9 |
| Citation | Hu L, et al. (2026) Obesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling. Cell Mol Immunol 23(3):301-314 |
| abstractText | Group 2 innate lymphoid cells (ILC2s) play crucial roles in maintaining adipose tissue homeostasis. Recent studies indicate that ILC2s are dysregulated in obesity. However, the regulatory mechanisms governing adipose tissue ILC2 function remain inadequately explored. In this study, we demonstrated that mechanistic target of rapamycin complex 1 (mTORC1) activity is impaired in adipose tissue ILC2s from obese mice and humans. Deletion of Raptor, a critical adaptor protein in mTORC1, results in reduced numbers of ILC2s and diminished type 2 cytokine production in ILC2s, leading to increased adipose tissue inflammation and insulin resistance. Mechanistically, mTORC1 signaling upregulates PPARgamma expression through HIF-1alpha, which promotes mitochondrial biogenesis and ST2 expression to sustain ILC2 metabolic and functional fitness. Together, our data identify mTORC1 as a crucial regulator that coordinates adipose tissue ILC2 metabolic and immunological homeostasis and prevents obesity-associated insulin resistance. |
