Franziska Roth‐Walter, Ioana Agache, Beatriz Cabanillas, Roberto Berni Canani, Pasquale Comberiati, Holger Garn, Cristina Gómez‐Casado, Karin Hufnagl, Ekaterina Khaleva, Gregorio P. Milani, Daniel Munblit, Nikolaos Douladiris, Liam O'Mahony, Frank A. Redegeld, Carmen Riggioni, Peter K. Smith, Betty C. A. M. van Esch, Εmilia Vassilopoulou, Carina Venter, Diego Peroni
Iron is essential for oxygen transport, energy metabolism, and immune regulation. Yet iron deficiency is the most common micronutrient disorder across all age groups, affecting nearly one quarter of the global population. Iron deficiency triggers nutritional immunity, a host defense mechanism that withholds and redistributes iron, contributing to increased morbidity and mortality. This review outlines normal iron physiology, distribution and absorption pathways and on the consequences of deficiency across body compartments, with particular attention to type 2-driven diseases. Beyond anemia, insufficient iron availability disrupts immune homeostasis by promoting type 2 inflammation, elevating IgE, and activating mast cells and eosinophils. Regulatory macrophages, the central hub of iron cycling, adopt an inflammatory, iron-sequestering state that reinforces malabsorption and redistribution. Epidemiology studies show higher iron-deficiency risk in allergic individuals; low maternal iron or early-life iron predisposes to eczema, wheeze, and asthma, while food-allergen elimination (notably cow's milk) further worsens anemia risk. Clinical evidence indicates that restoring iron status through diet, supplementation, or fortification lowers IgE levels, improves lung function, and alleviates symptoms of rhinitis, urticaria, and asthma. Iron may therefore represent a modifiable determinant of allergic disease development and severity. Integrating iron assessment and nutritional care into allergy management may reduce disease burden and slow the progression of allergic march.