Inhibitory effect of interleukin-3 on interleukin-2-induced cortisol release in the immunotherapy of cancer

J Biol Regul Homeost Agents. 1992 Oct-Dec;6(4):113-5.

Abstract

The stimulatory effect of IL-2 on cortisol rise represents an undesirable biological event during IL-2 cancer immunotherapy. At present, no cytokine has been proven to be able to counteract IL-2-induced cortisol increase. This study was carried out to evaluate the influence of IL-3 on IL-2 stimulation of cortisol secretion. Five lung cancer patients were investigated after IL-2 (3 x 10(6) IU s.c.), after IL-3 (1 mcg/kg b.w. i.v.) and after IL-3 plus IL-2, by administering IL-3 two hours before IL-2 injection. IL-2 significantly stimulated cortisol secretion. IL-3 alone had no effect on cortisol levels. The pretreatment with IL-3 completely neutralizes IL-2-induced cortisol release. These preliminary results would suggest that IL-3 may be associated with IL-2 during cancer immunotherapy to modulate the effect of IL-2 on the endocrine system.

MeSH terms

  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / therapy*
  • Female
  • Humans
  • Hydrocortisone / blood
  • Hydrocortisone / metabolism*
  • Immunotherapy
  • Interleukin-2 / pharmacology
  • Interleukin-2 / therapeutic use*
  • Interleukin-3 / pharmacology*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / therapy*
  • Male
  • Neoplasms / metabolism
  • Neoplasms / therapy*
  • Recombinant Proteins / pharmacology
  • Recombinant Proteins / therapeutic use

Substances

  • Interleukin-2
  • Interleukin-3
  • Recombinant Proteins
  • Hydrocortisone