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The dsRNA-mimetic poly (I:C) and IL-18 synergize for IFNgamma and TNFalpha expression

Amany Balah1, El-Sayed Akool, Malte Bachmann

  • 1Pharmazentrum Frankfurt/ZAFES, University Hospital Goethe-University, Theodor-Stern-Kai 7, Frankfurt am Main, Germany.

Biochemical and Biophysical Research Communications
|September 19, 2009
PubMed

Insights

Interleukin-18 (IL-18) and double-stranded RNA (dsRNA) synergistically boost pro-inflammatory cytokines like IFN-gamma and TNF-alpha. This potent immune response, mediated by TLR3, may contribute to tissue damage during viral infections.

Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • Interleukin-18 (IL-18) and dsRNA sensing are crucial for anti-viral immunity.
  • Understanding the cross-communication between IL-18 and dsRNA pathways is incomplete.

Purpose of the Study:

  • To investigate the synergistic effects of IL-18 and dsRNA on cytokine production.
  • To elucidate the molecular mechanisms underlying this synergy in human immune cells.

Main Methods:

  • Utilized human peripheral blood mononuclear cells (PBMCs) and KG1 cells.
  • Stimulated cells with IL-18 and poly (I:C) (a dsRNA mimetic).
  • Assessed cytokine production (IFN-gamma, TNF-alpha), NF-kappaB activation (IkappaB analysis, luciferase assays), and JNK activation.

Main Results:

  • Demonstrated potent synergy between IL-18 and poly (I:C) in inducing IFN-gamma and TNF-alpha.
  • Synergistic induction in KG1 cells involved Toll-like receptor 3 (TLR3).
  • Observed prolonged activation of NF-kappaB and JNK signaling pathways.

Conclusions:

  • IL-18 and dsRNA exhibit significant synergy in promoting pro-inflammatory cytokine production.
  • This synergy, potentially mediated by TLR3, involves sustained NF-kappaB and JNK activation.
  • Overwhelming cytokine induction during viral infections, driven by this synergy, could lead to tissue damage.

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