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

Abstract:

:Interleukin (IL)-18 bioactivity and dsRNA sensing by receptors of innate immunity are key components of anti-viral host defense. Despite extensive data on signal transduction activated by both pathways knowledge on cross-communication is incomplete. By using human PBMC and predendritic KG1 cells, as prototypic IL-18-responsive cellular models, we sought to assess cytokine production under the influence of IL-18 and the dsRNA-mimetic poly (I:C). Here, we report on potent synergy between both mediators concerning pro-inflammatory IFNgamma and TNFalpha production. KG1 data revealed that synergistic induction likely relied on TLR3 and was associated with prolonged/increased activation of NF-kappaB, as detected by IkappaB analysis and luciferase reporter assays, respectively. Moreover, extended activation of JNK was mediated by IL-18/poly (I:C). Although vital for innate immunity, overwhelming induction of inflammatory cytokines during viral infections poses the threat of serious collateral tissue damage. The stunning synergism inherent to IL-18/dsRNA-induced TNFalpha/IFNgamma detected herein may contribute to this pathological phenomenon.

authors

Balah A,Akool el-S,Bachmann M,Pfeilschifter J,Mühl H

doi

10.1016/j.bbrc.2009.09.040

subject

Has Abstract

pub_date

2009-11-27 00:00:00

pages

628-33

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(09)01828-2

journal_volume

389

pub_type

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