◀ Back to IL1B
IL1B — TLR2
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
IL1B
→
TLR2
(increases, IL1B Activity)
Aliprantis et al., EMBO J 2000*
Evidence: These data indicate that TLR2 is a novel 'death receptor' that engages the apoptotic machinery without a conventional cytoplasmic death domain. Through TLR2, BLP induces the synthesis of the precursor of the pro-inflammatory cytokine interleukin-1beta (IL-1beta).
-
OpenBEL Selventa BEL large corpus:
IL1B
→
TLR2
(increases, IL1B Activity)
Aliprantis et al., EMBO J 2000*
Evidence: Modified assertion
-
OpenBEL Selventa BEL large corpus:
TLR2
→
IL1B
(increases)
Evidence: Type-1 cytokines including IL-1?, TNF-? and IFN-? induced a strong up-regulation of TLR2 mRNA (Fig. 8) and protein expression that was most pronounced by the co-stimulation with TNF-? and IFN-? (Fig. 5).
Text-mined interactions from Literome
Oshikawa et al., Biochem Biophys Res Commun 2003
(Lung Diseases) :
The results demonstrated three patterns of gene expression : the
TLR2 and myeloid differentiation factor 88 ( MyD88 ) gene expressions were induced in AM in
response to lipopolysaccharide (LPS),
interleukin (IL)-1beta , or tumor necrosis factor-alpha or in the lung tissue of an LPS induced acute lung injury model ; the gene expressions of TLR1, -3, -6, CD14, and MD2 were unchanged ; and the TLR4 and TLR5 gene expressions were downregulated in AM following inflammatory stimuli
Sakai et al., BMC molecular biology 2004
:
Glucocorticoids synergistically enhance
IL-1beta induced
TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to dephosphorylation and inactivation of both MAPK JNK and p38, the negative regulators for TLR2 induction
Hajishengallis et al., Infect Immun 2005
:
Induction of
interleukin-1beta (IL-1beta) , IL-6, IL-8, or tumor necrosis factor alpha in human THP-1 cells by LT-IIaB or LT-IIbB was
inhibited by
anti-TLR2 but not by anti-TLR4 antibody
Su et al., Osteoarthritis Cartilage 2005
(Osteoarthritis, Knee) :
Expression and
regulation of
Toll-like receptor 2 by
IL-1beta and fibronectin fragments in human articular chondrocytes
Ozören et al., J Immunol 2006
:
Distinct
roles of
TLR2 and the adaptor ASC in
IL-1beta/IL-18 secretion in response to Listeria monocytogenes ... These results demonstrate that
TLR2 and ASC
regulate the secretion of
IL-1beta via distinct mechanisms in response to Listeria
Toshchakov et al., J Immunol 2007
(MAP Kinase Signaling System) :
TLR2- and TLR4-BB peptides ( BBPs )
inhibited NF-kappaB translocation and early
IL-1beta mRNA expression induced by LPS, and the lipopeptides S- [ 2,3-bis ( palmitoyloxy ) - ( 2-RS ) -propyl ] -N-palmitoyl- ( R ) -Cys-Ser-Lys ( 4 ) -OH ( P3C ) and S- [ 2,3-bis ( palmitoyloxy ) - ( 2-RS ) -propyl ] -Cys-Ser-Lys ( 4 ) -OH ( P2C )
Chang et al., Invest Ophthalmol Vis Sci 2007
(Acute Disease...) :
In contrast, significantly increased production of
IL-1beta in
response to
TLR2 stimulation was observed in patients with AAU ( P < 0.05 )
Li et al., J Immunol 2007
:
Alum induced
IL-1beta and IL-18 production was not
due to enhancement of
TLR signaling but rather reflected caspase-1 activation and in mouse dendritic cells occurred in a MyD88 independent fashion
Dinarello et al., Immunity 2007
(Inflammation) :
Secretion of the proinflammatory cytokine
IL-1beta requires caspase-1 and
Toll-like receptor ( TLR ) signaling
Kim et al., Immunol Lett 2007
(Arthritis, Rheumatoid...) :
TLR stimulation of RA-FLS also
induced the production of
IL-1beta and TNF-alpha to a lesser extent ; however, it had no effect on IL-17 production ... Inhibition of
TLR induced
IL-1beta production, which partially reversed the upregulation of RANKL induced by TLR ligands
Ferwerda et al., J Leukoc Biol 2007
(Crohn Disease) :
TLR induced TNF-alpha,
IL-1beta , and IL-10 production is mediated through MyD88, whereas Toll-IL-1R domain containing adaptor inducing IFN-beta ( TRIF ) promoted the release of IL-1beta
Villacres et al., J Viral Hepat 2008
(Hepatitis C, Chronic) :
To a lesser extent, tumour necrosis factor-alpha and
IL-1beta responses to
TLR stimulation were also compromised
Büchau et al., J Invest Dermatol 2008
:
Pimecrolimus also increased the functional capacity of keratinocytes to inhibit growth of Staphylococcus aureus and decreased
TLR2/6 induced expression of IL-10 and
IL-1beta
Wikén et al., J Clin Immunol 2009
(Sarcoidosis) :
Combined
TLR2 and NOD2 stimulation
induced a four-fold higher secretion of TNFalpha and a 13-fold higher secretion of
IL-1 beta in patients
Netea et al., Expert Opin Biol Ther 2008
(Inflammation) :
Monocytes can release active
IL-1 beta upon
stimulation with
TLR ligands alone
van de Veerdonk et al., J Infect Dis 2009
(Inflammation) :
The transcription of
IL-1beta was
induced through mannose receptor ( MR ),
Toll-like receptor (TLR) 2 , and dectin-1 but not through TLR4 and TLR9
Hurst et al., Immunobiology 2009
(Antiphospholipid Syndrome) :
Determination of expression-levels using real-time RT-PCR showed significantly augmented
TLR dependent
IL-1beta and caspase-1 expression
Jung et al., Immunol Lett 2009
(Arthritis, Experimental...) :
These data show that TLR2,
TLR4 , and TLR6 ligation synergistically
stimulates the production of TNF-alpha and
IL-1beta in IL-1Ra-deficient mice and suggest that TLRs contribute to the perpetuation of spontaneous arthritis in this animal model ... These data show that
TLR2 , TLR4, and TLR6 ligation synergistically
stimulates the production of TNF-alpha and
IL-1beta in IL-1Ra-deficient mice and suggest that TLRs contribute to the perpetuation of spontaneous arthritis in this animal model
Jie Zhao et al., Innate Immun 2009
(Aspergillosis...) :
Aspergillus fumigatus keratitis developed in Wistar rats, as evidenced by high SLE scores, influx of polymorphonuclear leukocytes ( PMNs ),
activation of
TLR2 and TLR4, and production of
IL-1beta and IL-10 over controls
Liu et al., PloS one 2009
:
TLR2/1 activation triggered
IL-1beta activity, involving the upregulation of both IL-1beta and IL-1 receptor, and downregulation of the IL-1 receptor antagonist
Lamkanfi et al., J Biol Chem 2009
(Inflammation) :
IL-1beta secretion further
required the
Toll-like receptor ( TLR ) adaptors MyD88 and TRIF, and partially relied on TLR2
Delaloye et al., PLoS Pathog 2009
:
Transcription of the
Il1b gene was markedly
impaired in
TLR2 ( -/- ) and MyD88 ( -/- ) BMDM, whereas mature and secreted IL-1beta was massively reduced in NALP3 ( -/- ) BMDMs or in human THP-1 macrophages with reduced expression of NALP3, ASC or caspase-1 by shRNAs
Kleinnijenhuis et al., Eur J Immunol 2009
:
In contrast,
TLR4 , TLR9 and TLR1 receptors are not
involved in
IL-1beta induction
Enstrom et al., Brain Behav Immun 2010
:
In particular, there was a marked increase in pro-inflammatory IL-1beta, IL-6, and TNFalpha responses following
TLR 2 , and
IL-1beta response following TLR 4 stimulation in monocyte cultures from children with ASD ( p < 0.04 )
Böni-Schnetzler et al., Endocrinology 2009
:
FFA induced
IL-1beta and KC expression in mouse islets was completely
dependent on the
IL-1R/Toll-like receptor ( TLR ) docking protein Myd88 and partly dependent on TLR2 and -4 ... FFA induced
IL-1beta and KC expression in mouse islets was completely dependent on the IL-1R/Toll-like receptor ( TLR ) docking protein Myd88 and partly
dependent on
TLR2 and -4
Mayer-Barber et al., J Immunol 2010
(Tuberculosis, Pulmonary) :
Caspase-1 independent
IL-1beta production is critical for host resistance to mycobacterium tuberculosis and does not
require TLR signaling in vivo
He et al., J Immunol 2010
(Chlamydia Infections...) :
TLR2 was
required for induction of
pro-IL-1beta , whereas the NLRP3/ASC was required for caspase-1 activation and pro-IL-1beta cleavage to produce mature IL-1beta