The engulfment of apoptotic cells by professional phagocytes can elicit anti-inflammatory mediators and dampen inflammation in the tissues. In Nature, Ravichandran and colleagues show that airway epithelial cells are able to engulf apoptotic targets and produce anti-inflammatory mediators. Deletion of the small GTPase Rac1 in airway epithelial cells results in defective clearance of apoptotic cells and less production of the anti-inflammatory cytokines IL-10 and TGF-β. In addition, airway epithelial cells are more sensitive to allergic airway inflammation. Rac1-deficient epithelial cells produce more IL-33 after allergen challenge, which increases the number of nuocyte-like cells in the lungs. These data indicate that airway epithelial cells are major players in modulating tolerance to common airway allergens.

Nature (12 December 2012) doi:10.1038/nature11714