Interleukin-2 primes eosinophil degranulation in hypereosinophilia and Wells' syndrome

Eur J Immunol. 2003 Apr;33(4):834-9. doi: 10.1002/eji.200323727.


Patients with hypereosinophilia frequently suffer from eosinophil-mediated damages of the heart, lungs, skin, and other organs, while some do not. The reason(s) for this difference is not known. We observed that eosinophils from most patients with hypereosinophilia express the alpha-chain of the IL-2 receptor (CD25), and that IL-2 enhances platelet-activating factor-stimulated release of eosinophil cationic protein from CD25-expressing but not from CD25-negative eosinophils. Such a "priming" effect has previously been described for eosinophil hematopoietins. These data suggest that patients with increased eosinophil surface CD25 expression are at higher risk of eosinophil degranulation and subsequent tissue damage when IL-2 is present at inflammatory sites.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asthma / immunology
  • Blood Proteins / metabolism
  • Cell Degranulation*
  • Dermatitis, Atopic / immunology
  • Drug Synergism
  • Eosinophil Granule Proteins
  • Eosinophilia / drug therapy
  • Eosinophilia / immunology*
  • Eosinophils / drug effects
  • Eosinophils / immunology*
  • Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology
  • Humans
  • Hypereosinophilic Syndrome / immunology
  • Interleukin-2 / pharmacology*
  • Interleukin-5 / pharmacology
  • Platelet Activating Factor / pharmacology
  • Receptors, Interleukin-2 / metabolism
  • Receptors, Interleukin-2 / physiology
  • Ribonucleases*
  • Syndrome


  • Blood Proteins
  • Eosinophil Granule Proteins
  • Interleukin-2
  • Interleukin-5
  • Platelet Activating Factor
  • Receptors, Interleukin-2
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Ribonucleases