Interleukin-18 activates NF-kappaB in murine T helper type 1 cells

Biochem Biophys Res Commun. 1997 May 19;234(2):454-7. doi: 10.1006/bbrc.1997.6665.


Interleukin-18 (IL-18) activated T helper type 1 (Th1) cells, OVA#4, and induced production of interleukin-2 (IL-2) in costimulation with anti-CD3 antibody. Upon stimulation with IL-18, IkappaB disappeared from cytoplasm and subsequently nuclear factor-kappaB (NF-kappaB) (p65) accumulated in the nucleus. Corresponding with that, DNA binding activity of NF-kappaB (p65 homodimer or p65/p50 heterodimer) was detected in the nucleus. In the transfection experiments, an IL-2 promoter-driven reporter construct showed the similar responsiveness against IL-18 to that of the intrinsic IL-2 gene, and a construct lacking kappaB site failed to respond to IL-18. These results suggest that IL-18 activates NF-kappaB and it is important for enhancement of IL-2 gene expression by Th1 cells stimulated with IL-18.

MeSH terms

  • Animals
  • Base Sequence
  • Biological Transport, Active
  • Cell Nucleus / metabolism
  • Clone Cells
  • Cytokines / pharmacology*
  • Cytoplasm / metabolism
  • DNA / metabolism
  • DNA Probes / genetics
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Genes, Reporter
  • I-kappa B Proteins*
  • Interleukin-18
  • Interleukin-2 / biosynthesis
  • Interleukin-2 / genetics
  • Lymphocyte Activation
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Rats
  • Th1 Cells / immunology*
  • Th1 Cells / metabolism*
  • Transcriptional Activation
  • Transfection


  • Cytokines
  • DNA Probes
  • DNA-Binding Proteins
  • I-kappa B Proteins
  • Interleukin-18
  • Interleukin-2
  • NF-kappa B
  • Nfkbia protein, rat
  • NF-KappaB Inhibitor alpha
  • DNA