Suppression of IL-2-induced SAA gene expression in mice by the administration of an IL-1 receptor antagonist

Cytokine. 1992 Nov;4(6):555-60. doi: 10.1016/1043-4666(92)90019-n.

Abstract

The hepatic acute phase response induced by the administration of interleukin (IL)-2 is most likely mediated by secondary cytokines. In this investigation, we examined the role of endogenous IL-1 in the synthesis of the hepatic acute phase protein serum amyloid A (SAA) during IL-2 treatment. The injection of IL-2 induced SAA gene expression in the liver. The concurrent administration of an IL-1 receptor antagonist (IL-1RA) markedly reduced hepatic SAA mRNA levels and, to a lesser extent, SAA protein levels in the serum. Although IL-1 is an inducer of IL-6 production, the administration of the IL-1RA had no effect on circulating IL-6 levels in IL-2-treated mice. These findings suggest that the production of IL-1 is an important factor in the induction of SAA mRNA in mice undergoing immunotherapy with IL-2.

MeSH terms

  • Animals
  • Female
  • Gene Expression / drug effects
  • Interleukin-1 / metabolism
  • Interleukin-2 / pharmacology*
  • Interleukin-6 / metabolism
  • Liver / metabolism
  • Mice
  • Mice, Inbred C3H
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptors, Interleukin-1 / antagonists & inhibitors*
  • Serum Amyloid A Protein / biosynthesis
  • Serum Amyloid A Protein / genetics*

Substances

  • Interleukin-1
  • Interleukin-2
  • Interleukin-6
  • RNA, Messenger
  • Receptors, Interleukin-1
  • Serum Amyloid A Protein