May '24: Article Alert!

While iron is an essential nutrient for many biological processes, its role in allergic asthma had not been well explored. We found that ILC2s — key drivers of airway inflammation — rapidly ramp up iron uptake when activated, and that blocking this process reduces their ability to expand and drive inflammation. Mechanistically, iron deprivation forces ILC2s to shift their energy metabolism in ways that dampen their inflammatory activity, and reducing iron availability in mouse models significantly alleviated allergic airway disease. These findings extended to human ILC2s, and in asthma patients, higher iron uptake by ILC2s was associated with worse lung function. Together, this work identifies cellular iron acquisition as a critical checkpoint in ILC2-driven inflammation and suggests that targeting iron metabolism could offer a new therapeutic avenue for allergic asthma.