Tumor necrosis factor-alpha enhances IL-15-induced natural killer cell differentiation

Biochem Biophys Res Commun. 2009 Sep 4;386(4):718-23. doi: 10.1016/j.bbrc.2009.06.120. Epub 2009 Jun 25.

Abstract

The differentiation of natural killer (NK) cells is regulated by various factors including soluble growth factors and transcription factors. Here, we have demonstrated that tumor necrosis factor-alpha (TNF-alpha) is a positive regulator of NK cell differentiation. TNF-alpha augmented the IL-15-induced expression of NK1.1 and CD122 in mature NK cells, and TNF-alpha alone also induced NK cell maturation as well as IL-15. TNF-alpha also increased IFN-gamma production in NK cells in the presence of IL-15. Meanwhile, mRNA expression of several transcription factors, including T-bet and GATA-3, was increased by the addition of TNF-alpha and IL-15. In addition, TNF-alpha increased nuclear factor-kappa B (NF-kappaB) activity in NK cells and inhibition of NF-kappaB impeded TNF-alpha-enhanced NK cell maturation. Overall, these data suggest that TNF-alpha significantly increased IL-15-driven NK cell differentiation by increasing the expression of transcription factors that play crucial roles in NK cell maturation and inducing the NF-kappaB activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Ly / biosynthesis
  • Cell Differentiation*
  • Interleukin-15 / pharmacology
  • Interleukin-15 / physiology*
  • Interleukin-2 Receptor beta Subunit / biosynthesis
  • Killer Cells, Natural / cytology*
  • Killer Cells, Natural / drug effects
  • Mice
  • Mice, Inbred C57BL
  • NK Cell Lectin-Like Receptor Subfamily B / biosynthesis
  • Tumor Necrosis Factor-alpha / pharmacology
  • Tumor Necrosis Factor-alpha / physiology*

Substances

  • Antigens, Ly
  • Il2rb protein, mouse
  • Interleukin-15
  • Interleukin-2 Receptor beta Subunit
  • Klrb1c protein, mouse
  • NK Cell Lectin-Like Receptor Subfamily B
  • Tumor Necrosis Factor-alpha