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IRF3 — TLR7
Text-mined interactions from Literome
Takahasi et al., Nat Struct Biol 2003
:
Transcription factor
IRF-3 is post-translationally
activated by
Toll-like receptor ( TLR ) signaling and has critical roles in the regulation of innate immunity
Schoenemeyer et al., J Biol Chem 2005
:
Here we show that in contrast to IRF3 and IRF7,
IRF5 is not a target of the TLR3 signaling pathway but is
activated by
TLR7 or TLR8 signaling
Cheng et al., J Immunol 2006
:
IRF-3 is expressed ubiquitously and is
activated by serine phosphorylation in response to viral infection or
TLR signaling
Lundberg et al., Blood 2007
(Inflammation) :
Furthermore,
TLR3 stimulation did not
activate NFkappaB, MAPKs, or
IRF-3 in DCs and MOs, but was able to do so in ECs and RA-SF
Xu et al., Mol Immunol 2008
:
PTP1B inhibits
TLR ligands induced
activation of MAPKs, NF-kappaB, and
IRF3 , furthermore, co-transfection of PTP1B inhibits both MyD88- and TRIF induced transcription of TNF-alpha and IFN-beta reporter genes in a dose dependent manner
Knödler et al., Leukemia 2009
:
IL-10 was found to downregulate MyD88, IRAK1 ( IL-1 receptor associated kinase ) and tumor necrosis factor receptor associated factor 6, essential adaptor molecules for TLR signaling, and to decrease
TLR induced nuclear expression of the nuclear factor-kappaB transcription factors c-Rel and Rel-B as well as
interferon regulatory factor (IRF)-3 and IRF-8
Seya et al., Immunol Rev 2009
(RNA Virus Infections) :
In response to RNA stimulation,
TLR3 recruits the Toll-interleukin 1 receptor domain ( TIR ) -containing adapter molecule 1 ( TICAM-1 ) adapter and
induces IRF-3 activation followed by IFN-beta promoter activation
Wu et al., Hepatology 2009
:
TLR stimulated expression of proinflammatory cytokines [ tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6) ], and activation of
IRF-3 was suppressed after up-regulation of HBV replication in HBV-Met cells
Atzei et al., J Biol Chem 2010
:
We now describe the first functional characterization of the human ortholog of Cactin ( hCactin ) and show that it acts as a negative regulator of TLRs. Overexpression of hCactin suppresses
TLR induced
activation of NF-?B and
interferon-regulatory factor transcription factors and induction of TLR-responsive genes, whereas knockdown of endogenous hCactin augments TLR induction of these responses
Tong et al., Cell Res 2012
:
NLRC5 ablation reduces MHC class I expression, and enhances IKK and
IRF3 phosphorylation in
response to
TLR stimulation or viral infection