Respiratory exposure to inhaled antigens leads to the formation of regionally compartmentalized lung-resident CD4+ memory TRM cells that, upon subsequent memory recall, secrete lineage-specific cytokines to orchestrate rapid innate immunity.37 TH17 TRM cell-derived IL-17A augments epithelial CXCL5 production to accelerate neutrophilic inflammation in the lungs during pneumonia.41,63,64 Given the rapidity of neutrophil responses (Figure 1E), we examined IL-17A and CXCL5 at the early time point of 8 h after allergen challenge. The gene discussed is CD4; the disease is susceptibility to pneumonia measurement.