IL‐4R signaling accelerates neutrophil aging. Circulating fresh neutrophils in healthy individuals can perform a variety of effector functions, including neutrophil extracellular trap (NET) release, reactive oxygen species (ROS) production, degranulation, and phagocytosis. An increase in the type 2 immune cytokines interleukin (IL)‐4 and IL‐13 affects phenotypical and functional properties of neutrophils and accelerates their aging. Aged neutrophils lose their granularity as well as ability to perform chemotaxis, phagocytosis, and NET release, whereas they are more prone to ROS production. The functional alterations are evident in type 2 immune diseases with increased IL‐4 and IL‐13 abundance. In mild‐to‐moderate disease manifestations, neutrophil counts are reduced in the affected tissues, but are found at normal levels in the blood. In severe type 2 immune skewing (e.g., by very high systemic concentrations of IL‐4), neutrophil counts can be reduced in blood and tissues.