When adult investigations revealed that neutrophilic inflammation and Th17 cells were crucial to illness, the relevance and functional contribution of eosinophils to the pathophysiology of severe asthma was called into doubt. Severe asthma in children was distinguished by eosinophilic inflammation, atopic sensitization, and airway remodeling. In children with severe illness who were given high-dose steroids, neutrophils, Th17, and Th2 cytokines were seldom found, contrary to adult findings. Type 2 innate lymphoid cells (ILCs), which were activated by the epithelial cytokine interleukin (IL)-33 and produced the Th2 cytokines IL-5 and IL-13, were found to be significant in regulating asthma, and ILCs, in particular, played a role in controlling eosinophil homeostasis. The discovery of a direct relationship between IL-33, airway remodeling, and steroid resistance in children with severe asthma showed that steroid-resistant eosinophilia might be mediated by ILCs rather than traditional Th2 cells. Data from children with severe asthma demonstrated that adult findings cannot be generalized to children and that steroid-resistant eosinophilic inflammation appeared to be fundamental to the etiology of pediatric illness. Age-appropriate experimental models and the utilization of pediatric airway samples were crucial for understanding the underlying processes and discovering potential treatment targets.