Anti‐inflammatory effects of the <scp>GAG</scp>‐binding <scp>CXCL</scp>9(74‐103) peptide in dinitrofluorobenzene‐induced contact hypersensitivity in mice

Abstract

The CXCL9(74-103) peptide inhibited dinitrofluorobenzene-induced infiltration of neutrophils and neutrophil-dependent inflammation in ears. Therefore, CXCL9(74-103) may be a lead molecule for the development of therapeutic peptides or peptide derivatives that compete with functional chemokines for GAG binding.