An interleukin 5 mutant distinguishes between two functional responses in human eosinophils

J Exp Med. 1997 Jul 7;186(1):121-9. doi: 10.1084/jem.186.1.121.

Abstract

Interleukin 5 (IL-5) is the key cytokine involved in regulating the production and many of the specialized functions of mature eosinophils including priming, adhesion, and survival. We have generated a point mutant of human IL-5, IL-5 (E12K), which is devoid of agonist activity in both a TF-1 cell proliferation assay and a human eosinophil adhesion assay. However, IL-5 (E12K) is a potent and specific antagonist of both these IL-5-dependent functional responses. In both receptor binding and cross-linking studies the wild-type and IL-5 (E12K) mutant exhibit virtually identical properties. This mutant protein was unable to stimulate tyrosine phosphorylation in human eosinophils, and blocked the phosphorylation stimulated by IL-5. In contrast, IL-5 (E12K) is a full agonist in a human eosinophil survival assay, although with reduced potency compared to the wild-type protein. This IL-5 mutant enables us to clearly distinguish between two IL-5-dependent functional responses and reveals distinct mechanisms of receptor/cellular activation.

MeSH terms

  • Cells, Cultured
  • Eosinophils / immunology*
  • Humans
  • Interleukin-5 / genetics
  • Interleukin-5 / immunology*
  • Mutation
  • Receptors, Interleukin / immunology
  • Receptors, Interleukin-5
  • Signal Transduction / genetics
  • Signal Transduction / immunology

Substances

  • Interleukin-5
  • Receptors, Interleukin
  • Receptors, Interleukin-5