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IL1A — TLR4

Text-mined interactions from Literome

Netea et al., J Infect Dis 2002 (Candidiasis) : Production of tumor necrosis factor (TNF) and interleukin (IL)-1alpha and IL-1beta by mouse macrophages in response to C. albicans stimulation was not affected by TLR4 , and the candidacidal capacities of the neutrophils and macrophages of C3H/HeJ mice were normal
Yamamoto et al., Nature 2004 : Transcription of IkappaBzeta is rapidly induced by stimulation with TLR ligands and interleukin-1 (IL-1)
Szczepański et al., Eur Arch Otorhinolaryngol 2006 (Cholesteatoma, Middle Ear...) : TLR-ligand binding results in cell signal transduction and subsequent production of various proinflammatory cytokines such as IL-1 and TNF-alpha
Abdollahi-Roodsaz et al., Arthritis Rheum 2007 (Arthritis...) : In the present study, we demonstrate for the first time that inhibition of TLR-4 suppresses the severity of experimental arthritis and results in lower IL-1 expression in arthritic joints
van Beelen et al., Immunity 2007 (Bacterial Infections...) : MDP enhanced obligate bacterial Toll-like receptor ( TLR ) agonist induction of IL-23 and IL-1 , which promoted IL-17 expression in T cells
Shoma et al., Infect Immun 2008 : When macrophages were stimulated with rPLY, the production of IL-1alpha , IL-1beta, and IL-18 was strongly induced in a TLR4 dependent manner, whereas lipopolysaccharide, a canonical TLR4 agonist, hardly induced these cytokines
Cha et al., Ann Thorac Surg 2008 (Myocardial Reperfusion Injury) : This study examined whether TLR4 regulates TNF-alpha and interleukin (IL)-1beta peptide production during global ischemia/reperfusion and whether TLR4 signaling influences postischemic cardiac function through TNF-alpha and IL-1beta
Croker et al., Proc Natl Acad Sci U S A 2008 (Autoimmune Diseases...) : TLR induced TNF and IL-1 production are normal in macrophages derived from spin mice
Böni-Schnetzler et al., Endocrinology 2009 : We conclude that FFA and TLR stimulation induce proinflammatory factors in islets and that IL-1RI engagement results in signal amplification
Deopurkar et al., Diabetes Care 2010 (Inflammation) : Indexes of inflammation including nuclear factor-kappaB (NF-kappaB) binding, and the expression of SOCS3, tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-1beta in MNCs, increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS concentrations increased only after cream intake
Dewamitta et al., Infect Immun 2010 : The Toll-like receptor ( TLR ) /MyD88 signaling pathway was exclusively required for the expression of pro-IL-1 alpha , independently of LLO mediated cytoplasmic entry of L. monocytogenes
Chávez-Sánchez et al., Lipids in health and disease 2010 : The activation of CD14, TLR4 , and TLR2 by mmLDL induces IL-1ß , IL-6, and IL-10 secretion in human monocytes and macrophages ... Blocking CD14 in monocytes inhibited secretion of interleukin (IL)-1ß ( 72 % ), IL-6 ( 58 % ) and IL-10 ( 63 % ), and blocking TLR4 inhibited secretion of IL-1ß by 67 %, IL-6 by 63 % and IL-10 by 60 %
Dasu et al., Am J Physiol Endocrinol Metab 2011 (Diabetes Mellitus, Type 2...) : Silencing TLR2, TLR4 , and p47phox with small inhibitory RNAs ( siRNAs ) significantly reduced superoxide release, NF-?B activity, IL-1ß , and MCP-1 secretion in HG and palmitate treated THP-1 cells
Embry et al., Science signaling 2011 : In addition, we elucidated the contributions of MyD88 and TRIF to priming of the NLRP3 inflammasome and demonstrated that TRIF biased TLR4 activation by MLA was responsible for the defective production of mature IL-1ß
Carta et al., J Biol Chem 2011 : TLR engagement induces an effective redox response with increased ROS generation followed by a sustained antioxidant response, parallelled by efficient IL-1ß secretion
Das et al., Immunol Cell Biol 2012 (Leishmaniasis, Visceral) : In this report, we demonstrated that later stages of L. donovani infection rendered tolerance to macrophages, leading to incapability for the production of inflammatory cytokines like tumor necrosis factor (TNF)-a and interleukin (IL)-1ß in response to TLR stimulation
Besnard et al., Journal of molecular cell biology 2012 (Pneumonia) : The production of pro-IL-1ß requires a toll-like receptor (TLR) 4 signal which is provided by the allergen
Xia et al., J Pineal Res 2012 (Inflammation) : As expected, melatonin inhibited TLR4 mediated tumor necrosis factor alpha ( TNF-a ), interleukin (IL)-1ß , IL-6, IL-8, and IL-10 in LPS stimulated macrophages
den Dunnen et al., Blood 2012 (Bacterial Infections...) : First, TLR-Fc?RIIa costimulation strongly increased transcription of pro-IL-1ß and IL-23p19
Villacres et al., J Infect Dis 2012 (HIV Infections...) : Peripheral blood mononuclear cells ( PBMCs ) obtained at baseline were used to measure interleukin 1ß (IL-1ß) , interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 12 (IL-12), and tumor necrosis factor a (TNF-a) responses to Toll-like receptor (TLR) 3 and TLR4 stimulation
Kavathas et al., Mucosal Immunol 2013 : In addition, we demonstrate that Ct-induced IL-1ß production and secretion by the trophoblast is independent of TLR2, TLR4 , MyD88, and the Nalp3/ASC inflammasome
Lee et al., Invest Ophthalmol Vis Sci 2012 (Disease Models, Animal...) : TLR4 inhibition decreased the severity of CFS and significantly reduced the mRNA expression of IL-1ß , IL-6, and TNF
Perugorria et al., Hepatology 2013 (Liver Cirrhosis...) : KCs lacking Tpl2 display defects with TLR induction of cytokines interleukin (IL)-1ß , IL-10, and IL-23
Gupta et al., Cell Signal 2013 (Glioma...) : IL-1ß increased HLA-G and Toll like receptor 4 (TLR4) expression in a HIF-1a dependent manner ... IL-1ß increased HMGB1 expression and its interaction with TLR4 ... Importantly, ß-defensin-3 prevented IL-1ß induced HLA-G, TLR4 , HMGB1 expression and release of pro-inflammatory mediators
He et al., J Immunol 2013 : Furthermore, they challenge the idea that the ATP-P2X7 axis is critical for TLR induced IL-1ß production via the Nlrp3 inflammasome in vivo
Wu et al., PloS one 2013 : We showed that the hADSCs expressed Toll-like Receptors (TLR) 1, TLR2, TLR3, TLR4 , and TLR6 and that lipopolysaccharide (LPS) significantly induced the production of pro-inflammatory cytokines ( Cyclooxygenase-2 (Cox-2), Interleukin-1ß (IL-1ß) , Interleukin-6 (IL-6), and Interleukin-8 (IL-8) )
Mulla et al., PloS one 2013 (Antiphospholipid Syndrome) : We recently demonstrated in human first trimester trophoblast cells that anti-ß2GPI antibodies ( Abs ) induce the secretion of IL-1ß in a Toll-like receptor 4 (TLR4) dependent manner ... Furthermore, aPL stimulated the production of uric acid in a TLR4 dependent manner ; and inhibition of uric acid prevented aPL induced IL-1ß production by the trophoblast
Waldschmidt et al., Vet Immunol Immunopathol 2013 : TLR 4 stimulation with 100ng/mL of LPS during 3h increased TNFa, IFNß, and Il-1ß expression