GPX4-dependent ferroptosis governs ILC2 homeostasis and colitis progression - PubMed
3 months ago
- #Inflammatory Bowel Disease
- #ILC2
- #Ferroptosis
- ILC2s are vulnerable to ferroptosis, indicated by ferroptosis signature genes and lipid peroxidation accumulation.
- Ablation of GPX4 in ILC2s leads to ferroptosis and diminished immune responses.
- IFN-γ signaling enhances oxidative stress, contributing to GPX4 ablation-induced ILC2 ferroptosis.
- Mice with GPX4-deficient ILC2s show increased susceptibility to DSS-induced colitis.
- IBD patients' ILC2s exhibit reduced GPX4 expression and increased lipid peroxidation.
- Ferroptosis plays a critical role in ILC2 homeostasis and offers therapeutic potential for inflammatory disorders.