Melatonin suppresses ILC2-driven airway hyperreactivity via glutathione-dependent metabolic reprogramming - Takeaways - MDSpire

Melatonin suppresses ILC2-driven airway hyperreactivity via glutathione-dependent metabolic reprogramming

  • By

  • Jafar Cain

  • Benjamin P. Hurrell

  • Stephen Shen

  • Paul Speliakos

  • Omid Akbari

  • May 11, 2026

  • 0 min

Share

  • 1

    Melatonin regulates ILC2 metabolism and function, reducing eosinophilia and airway hyperreactivity in murine models of allergic asthma.

  • 2

    Melatonin's effects on ILC2s occur independently of canonical receptors, enhancing pentose phosphate pathway activity and glutathione accumulation.

  • 3

    NRF2 activation is necessary and sufficient to restrain ILC2 effector function, highlighting its role in modulating airway inflammation.

  • 4

    Primary human ILC2s show conserved responses to melatonin, including NRF2 activation and reduced type 2 cytokine production.

  • 5

    The melatonin-NRF2-glutathione axis represents a potential therapeutic target for managing airway inflammation in allergic asthma.

Original Source(s)

Melatonin suppresses ILC2-driven airway hyperreactivity via glutathione-dependent metabolic reprogramming

  • by Jafar Cain, Benjamin P. Hurrell, Stephen Shen, Paul Speliakos, Omid Akbari

  • May 11, 2026

Related Content

AAP Updates Pediatric Office Emergency Readiness

Guidance addresses office readiness, recommended equipment and medications, and team communication processes for infrequent but high-acuity emergencies.

Fibrinogen-like protein 2 regulates inflammatory and metabolic reprogramming of airway smooth muscle cells through PI3K/Akt activation

Top 10 States With Rising Demand for Physicians

These 10 states report physician shortages, projected physician supply gaps, or physician-to-population ratios below national benchmarks.