◀ Back to TLR4
IFNB1 — TLR4
Text-mined interactions from Literome
Schilling et al., J Immunol 2002
:
TLR4 dependent induction of IL-6 expression did require Toll-IL-1R domain containing adapter protein ( TIRAP ) /MyD88 adapter-like (Mal), but unlike iNOS and IP-10, it did not
require the expression of
IFN-beta
Karaghiosoff et al., Nat Immunol 2003
(Shock, Septic) :
Toll-like receptor-4 activation by lipopolysaccharide (LPS)
induces the expression of
interferon-beta (IFN-beta) in a MyD88 independent manner
Kaisho et al., Curr Mol Med 2003
:
TLR2 can not induce IFN-alpha or IFN-beta, but
TLR4 can
lead to
IFN-beta production ... Meanwhile,
TLR3 , TLR7, and TLR9 can
induce both IFN-alpha and
IFN-beta
Sakaguchi et al., Biochem Biophys Res Commun 2003
:
Although much has been studied about the activation of the transcription factor IRF-3 and
induction of
IFN-beta gene by the LPS mediated
TLR4 signaling, definitive evidence is missing about the actual role of IRF-3 in LPS responses in vitro and in vivo
Toshchakov et al., J Endotoxin Res 2003
:
The data presented show that activation of
TLR4 by Escherichia coli LPS results in an MyD88 independent, TIRAP/Mal dependent signaling pathway that, in turn,
leads to early induction of
interferon-beta (IFN-beta)
Oshiumi et al., J Biol Chem 2003
:
We conclude that for
LPS-TLR4 mediated activation of
IFN-beta , the adapter complex of TICAM-2 and TICAM-1 plays a crucial role
Coccia et al., Eur J Immunol 2004
:
TLR-9 stimulation by CpG DNA induced the expression of all IFN-alpha, -beta, -omicron and -lambda subtypes in pDC, whereas
TLR-4 stimulation by LPS, or TLR-3 stimulation by poly I:C,
induced only
IFN-beta and IFN-lambda gene expression in MDDC
Hirotani et al., Biochem Biophys Res Commun 2005
:
TLR4 activates intracellular signaling pathways via TIR domain containing adaptor molecules, MyD88, and Toll/IL-1 domain containing adaptor
inducing IFN-beta ( TRIF )
Aksoy et al., Eur J Immunol 2005
:
In the same models of DC activation, PI3K inhibition increased DNA binding activity of NF-kappaB, but not interferon response factor (IRF)-3, the key transcription factors required for
TLR mediated
IFN-beta synthesis
Yang et al., Immunity 2005
(Virus Diseases) :
In contrast,
IFN-alpha/beta and -lambda were
induced normally by TLR-3 and
TLR-4 agonists
Machida et al., J Virol 2006
(Hepatitis C) :
The increased
IFN-beta and IL-6 production was
mediated by
TLR4 induction, since the introduction of the small interfering RNA against TLR4 specifically inhibited the HCV induced cytokine production
Broad et al., Immunology 2007
:
Furthermore, the production of
interferon-beta (IFN-beta) following stimulation of TLR3 or -4, which is MyD88 independent, was
increased by prior activation of
TLR4 , -5, -7 or -9
Koga et al., J Immunol 2006
(Chagas Disease) :
TLR dependent induction of
IFN-beta mediates host defense against Trypanosoma cruzi ... These findings suggest that
TLR dependent expression of
IFN-beta is involved in resistance to T. cruzi infection through the induction of IRG47
Colonna et al., Eur J Immunol 2007
:
TLR-3 and
TLR-4 induce
IFN-beta by activating IRF-3 ; TLR-9 induces IFN-alpha and IFN-beta through IRF-7, at least when engaged by type A CpG oligonucleotides ( CpG-A ) in plasmacytoid DC ( pDC ) ... These results demonstrate that
TLR induce IFN-alpha or
IFN-beta responses by activating distinct IRF, depending on the TLR ligand and the cell type
Wang et al., Blood 2007
:
Here we demonstrate that Rab7b can negatively
regulate lipopolysaccharide (LPS) induced production of tumor necrosis factor (TNF)-alpha, IL-6, nitric oxide, and
IFN-beta , and potentiate LPS induced activation of mitogen activated protein kinase, nuclear factor kappaB, and IFN regulatory factor 3 signaling pathways in macrophages by promoting the degradation of
TLR4
Bafica et al., J Immunol 2007
(Endotoxemia) :
Together, these observations indicate that in LPS stimulated murine macrophages LRG47 is induced by
IFN-beta and negatively
regulates TLR4 signaling to prevent excess proinflammatory cytokine production and shock
Rudd et al., Viral Immunol 2007
(Respiratory Syncytial Virus Infections) :
The data demonstrate that production of
IFN-beta , but not IFN-alpha, in RSV infected wild type DCs
promotes chemokine production and
toll-like receptor ( TLR ) expression, while limiting IL-12 production
Eskan et al., J Immunol 2008
:
In this study, we demonstrate that S1P1 and
TLR4 , acting in unison,
play an important role in
IFN-beta expression at the protein and mRNA level in HGECs ... Our data show that triggering TLR4 increases S1P1, such that both
TLR4 and S1P1
acting through PI3K enhancement of IFN-regulatory factor 3 activation increase
IFN-beta expression in epithelial cells
Cross et al., J Immunol 2008
:
CD45 regulates
TLR induced proinflammatory cytokine and
IFN-beta secretion in dendritic cells ... CD45 affected
TLR4 induced proinflammatory cytokine and
IFN-beta secretion and TLR4 activated CD45-null DCs had a reduced ability to activate NK and Th1 cells to produce IFN-gamma
Shingai et al., Int Immunol 2008
:
Soluble G protein of respiratory syncytial virus inhibits
Toll-like receptor 3/4 mediated
IFN-beta induction
Jiang et al., Virology 2008
(Hemorrhagic Fever with Renal Syndrome) :
The increased
IFN-beta , IL-6 and TNF-alpha production was
mediated by
TLR4 induction, since the introduction of the small interfering RNA against TLR4 specifically inhibited the HTNV induced cytokine production ... In conclusion, HTNV infection directly
induces TLR4 expression and thereby enhanced production of
IFN-beta , IL-6 and TNF-alpha, which may contribute to the host 's innate immune response
Cao et al., Nat Immunol 2008
:
Thus, mTOR signaling is crucial in
TLR mediated
IFN-alpha/beta responses by pDCs
Ciencewicki et al., J Interferon Cytokine Res 2009
:
Interestingly, although influenza infection results in
IFN-beta release both toward the apical and basolateral sides of the epithelium,
TLR3 expression is only
enhanced in cells stimulated with IFN-beta from the basolateral side
Chang et al., Virology 2009
:
We further demonstrate that the HCMV derived interleukin 10 (IL-10) homolog functions similar to cellular IL-10 and broadly inhibits
TLR induced transcriptional activation of
IFN-alpha/beta genes in plasmacytoid dendritic cells ( PDCs ), a major type I IFN-producer in vivo that is highly resistant to HCMV infection in vitro
Yu et al., J Allergy Clin Immunol 2009
(Common Variable Immunodeficiency) :
These TLR defects are restricted because CVID PBMCs stimulated with TLR ligands produced normal amounts of TNF-alpha, IL-6, and IL-12
; TLR3 mediated expression of
IFN-beta by CVID fibroblasts was normal
Renneson et al., Eur J Immunol 2009
:
Neonatal myeloid DC were shown to be deficient in
IFN-beta and IL-12 synthesis in
response to
TLR triggering
Marsh et al., J Neurosci 2009
(Infarction, Middle Cerebral Artery...) :
TLR4 can
induce both
IFNbeta and interferon stimulated genes through its adapter molecule Toll/interleukin receptor domain containing adaptor inducing IFNbeta ( TRIF ) and the IRF3 transcription factor
Kaiser et al., J Exp Med 2009
:
Here, we investigated the role of the TPL-2 signaling pathway in
TLR induction of
interferon-beta (IFN-beta) and interleukin-10 (IL-10) in these cell types
Wang et al., J Clin Invest 2009
(Enterocolitis...) :
In contrast,
TLR3 activated expression of
IFN-beta , a TRIF dependent response, was normal in Hfe KO macrophages and was unaffected by iron chelation
Burns et al., J Immunol 2010
(Bacteroidaceae Infections) :
Proinflammatory cytokine production in response to P. gingivalis infection depends on TLR2, but it does not require MyD88 or
TLR/IL-1R-domain containing adaptor
inducing IFN-beta
Gabhann et al., J Immunol 2010
:
SHIP-1-deficient macrophages display enhanced
TLR induced
IFN-beta production, and overexpression of SHIP-1 negatively regulates the ability of TLR3 and its adaptor, Toll/IL-1 receptor domain containing adaptor inducing IFN-beta, to induce IFN-beta promoter activity, indicating that SHIP-1 negatively regulates TLR induced IFN-beta production
Hoshino et al., J Immunol 2010
:
Importantly, IKKalpha was dispensable for
IFN-beta gene
upregulation by
TLR4 signaling
He et al., J Cell Biochem 2010
:
The activation of
TLR4 by LPS modulated the expression of TLRs, induced the phosphorylation of NF-kappaB, P38, and ERK42/44, and
up-regulated the gene expression of cytokines IL-8, IFN-alpha,
IFN-beta , and TNF-alpha, suggesting EPCs expressed functional TLR4