Interleukin-4 down-regulates Sendai virus-induced production of interferon-alpha and -beta in human peripheral blood monocytes in vitro

Scand J Immunol. 1992 Feb;35(2):167-75. doi: 10.1111/j.1365-3083.1992.tb02847.x.


Recombinant interleukin-4 (rIL-4) caused a 65-70% reduction of the interferon-alpha (IFN-alpha) and -beta production induced by Sendai virus (SV) in human peripheral blood monocytes in vitro. Significant inhibition was seen at concentrations as low as 0.1 ng/ml. The rIL-4 also reduced levels of IFN-alpha and -beta mRNA by 60% and 67%, respectively, as well as the frequency of IFN-alpha and -beta mRNA-containing cells by 65% and 54%, respectively. The frequency of IFN-alpha/beta mRNA-containing cells was inhibited by rIL-4 throughout the whole course of induction by SV. IL-4 caused a shift of the grain count distribution towards less heavily labelled cells, suggesting an inhibitory effect of rIL-4 on most IFN-alpha/beta mRNA-containing cells. Antibodies to rIL-4 did not influence the normal IFN-alpha/beta response induced by SV, but abolished the inhibitory effect of the rIL-4. When rIL-4 was added to cells 4 h after start of stimulation by SV, at which time much mRNA has accumulated but little IFN-alpha/beta has been secreted, no inhibition of the IFN-alpha/beta production by rIL-4 was seen. IFN-gamma had only a minor reversing effect on the rIL-4 inhibition, but if cells were precultivated in medium with or without IFN-gamma for 6 h before SV induction, rIL-4 paradoxically enhanced the IFN-alpha/beta response. Our results suggest that rIL-4 inhibits an early step of IFN-alpha/beta induction in monocytes, at the level either of transcription of IFN-alpha/beta genes or of the processing or stability of mRNA. The IL-4 effects may however depend on the state of activation of the monocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / genetics
  • Blotting, Northern
  • DNA Probes
  • Down-Regulation
  • Humans
  • Interferon-alpha / antagonists & inhibitors*
  • Interferon-alpha / genetics
  • Interferon-beta / antagonists & inhibitors*
  • Interferon-beta / genetics
  • Interferon-gamma / pharmacology
  • Interleukin-4 / pharmacology*
  • Macrophage Activation
  • Monocytes / immunology*
  • Parainfluenza Virus 1, Human / immunology*
  • RNA, Messenger / metabolism
  • Recombinant Proteins / pharmacology


  • Actins
  • DNA Probes
  • Interferon-alpha
  • RNA, Messenger
  • Recombinant Proteins
  • Interleukin-4
  • Interferon-beta
  • Interferon-gamma