May '26: Paper Alert!

Allergic asthma involves nighttime worsening of symptoms driven by immune cell activity, but the metabolic mechanisms behind this daily variation are not well understood. Our research reveals that melatonin — best known as a sleep hormone — acts as an unexpected regulator of Group 2 innate lymphoid cells (ILC2s), key drivers of airway inflammation. In mouse models of allergic asthma, melatonin reduced airway inflammation and hyperreactivity by reprogramming ILC2 metabolism to boost antioxidant defenses through the NRF2-glutathione pathway. Crucially, human ILC2s responded to melatonin in the same way, highlighting the clinical potential of these findings. This work identifies a novel melatonin-NRF2-glutathione metabolic axis as a natural brake on airway inflammation, pointing to redox metabolism as a promising therapeutic target for allergic asthma. 

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