In conclusion, antagonistic peptides that specifically bind to the first and second extracellular loops of CCR5 suppress the development of airway inflammation in asthmatic mice, possibly by inhibiting the CCR5-mediated IL-23/Th17 signaling pathway, and a variety of mechanisms might be responsible for the HY peptide-mediated suppression of airway inflammation. The gene discussed is CCR5; the disease is inflammatory response.