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Blockade of NKp46⁻ CCR6⁻ ILC3 autophagy protects against necrotizing enterocolitis by restoring energy metabolism balance in mice
Blocking a specific immune cell process protects mice from severe intestinal disease by restoring energy balance
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Abstract
In neonatal necrotizing enterocolitis (NEC), NKp46⁻CCR6⁻ ILC3s are identified as the dominant pathogenic subset that drives disease through IL-17 A secretion.
- IL-17 A secreted by DN ILC3s disrupts intestinal barrier integrity, contributing to NEC.
- Atg5 activation of autophagy in DN ILC3s is crucial during the development of NEC.
- Conditional knockout of Atg5 in RORγt⁺ cells reduces DN ILC3 accumulation and IL-17 A production, mitigating NEC.
- Atg5 deficiency leads to decreased HIF-1α activity and shifts DN ILC3 metabolism from glycolysis to fatty acid oxidation.
- Phosphatidylcholine, a metabolite resulting from Atg5-mediated autophagy, suppresses DN ILC3-driven inflammation and restores metabolic balance.
- Human NEC tissues show increased proportions of ILC3s, autophagic activity, and secretion of IL-17 A/IL-22.
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