Regulation of IFN-gamma mRNA production in murine natural killer cells

Int Immunol. 1995 Apr;7(4):575-82. doi: 10.1093/intimm/7.4.575.

Abstract

We have previously reported that large, presumably in vivo activated, B cells stimulate murine natural killer (NK) cells to secrete increased levels of IFN-gamma. In order to further understand the mechanism of IFN-gamma induction, we compared the regulation of IFN-gamma mRNA production after stimulation of NK cells with either B lymphocytes or phorbol myristate acetate (PMA)+ionomycin. Here we show that stimulation of NK cells by either stimuli results increase in IFN-gamma mRNA, albeit with different kinetics. Although the induction requires new RNA synthesis, we could not detect increased transcription of the IFN-gamma gene after stimulation. Measurement of the rate of mRNA degradation after IFN-gamma mRNA has accumulated demonstrates that this mRNA is more stable than IFN-gamma mRNA from unstimulated NK cells. Together, these results suggest that the increase in IFN-gamma mRNA and protein in NK cells, stimulated by B cells or PMA+ionomycin, results from stabilization of pre-existing IFN-gamma message. Our results also suggest that induction of the factor which stabilizes the mRNA, although as yet unknown, requires new RNA synthesis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • B-Lymphocytes / immunology
  • Female
  • Half-Life
  • Interferon-gamma / biosynthesis*
  • Interferon-gamma / genetics
  • Interleukin-2 / physiology
  • Ionomycin / pharmacology
  • Killer Cells, Natural / metabolism*
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Mice, SCID
  • RNA, Messenger / biosynthesis*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic / drug effects

Substances

  • Interleukin-2
  • RNA, Messenger
  • Ionomycin
  • Interferon-gamma
  • Tetradecanoylphorbol Acetate