ライフサイエンスコーパス: TLR4

1 the membrane receptor Toll-like receptor 4 (TLR4).

2 c neurons that express Toll-like receptor 4 (TLR4).

3 es to broadly reprogram responses induced by TLR4.

4 highest concentrations of ATIs that activate TLR4.

5 utes to OA progression, mediated by TLR2 and TLR4.

6 macrophages, followed by its endocytosis via TLR4.

7 ta production downstream of the LPS receptor TLR4.

8 ue to the inability of RESTV GP to stimulate TLR4.

9 inhibitor, indicating that MfP acts through TLR4.

10 hat directly and cooperatively interact with TLR4.

11 ell-line it was confirmed that LCM activated TLR4.

12 eparative effects in a mechanism mediated by TLR4.

13 ical blood flow compared to mice with normal TLR4.

14 phase, Tregs were significantly increased in TLR4(0/0) mice as compared to wild-type mice, whereas Tr

15 exhibited a delayed recovery as compared to TLR4(0/0) mice, which was because of an impaired T helpe

16 led a major role for TLR2, a lesser role for TLR4, a supplementary role for C5aR, and no apparent act

17 ly suppressed the release of IL-27p28 in LPS/TLR4-activated macrophages, which was independent of alp

18 dern gluten-containing staples had levels of TLR4-activating ATIs that were as much as 100-fold highe

19 Recent studies implicate TLR4 activation and oxidative stress in cardiovascular d

20 in a dose-dependent way, the LPS-stimulated TLR4 activation and TLR4-dependent cytokine production i

21 50 < 1 muM) and prevented DC maturation upon TLR4 activation by ultrapure lipopolysaccharide (LPS).

22 Therefore, FP7 can antagonize TLR4 activation in vitro and protect mice from severe in

23 PI3Kgamma for Akt-dependent signaling during TLR4 activation to limit the production of the proinflam

24 otentiates cytokine expression downstream of TLR4 activation via p38 MAPK and SGK1.

25 duction of PI3K/AKT signaling in response to TLR4 activation, leading to hyperinflammation, a hallmar

26 ved lipoproteins and LPS to inhibit TLR2 and TLR4 activation, respectively.

27 iator of T/HS-induced ALI through macrophage TLR4 activation.

28 suggests CIRP directly induces ER stress via TLR4 activation.

29 nsory neurons, and behavioral changes due to TLR4 active metabolite, morphine-3-glucuronide (M3G) exp

30 ed mouse tumors using HMGN1, a DC-activating TLR4 agonist capable of inducing anti-tumor immunity.

31 e absence of TLR2, STING, or the addition of TLR4 agonist has no effect.

32 onocyte/macrophage cells challenged with the TLR4 agonist LPS and TLR2 agonists lipoteichoic acid and

33 2 agonists Pam3CSK4 or FSL-1, as well as the TLR4 agonist LPS in the absence of additional ATP.

34 contrast, IL-1beta release stimulated by the TLR4 agonist LPS is independent of both pannexin-1 and P

35 ess TSLPR and CD127 mRNAs in response to the TLR4 agonist LPS, their responsiveness to TSLP is poorly

36 oxide causes pro-inflammatory activation and TLR4 agonists act preferentially via caveolae-derived en

37 Toll-like receptor 1/2 (TLR1/2), TLR2/6, and TLR4 agonists were impaired in the fibroblasts and leuko

38 tivated in peritoneal B cells in response to TLR4 agonists, neither MSKs nor CREB are required for IL

39 ng Lewis lung carcinoma (LLC), and targeting TLR4 alone effectively abrogate muscle wasting.

40 In mice with liver inflammation, we found TLR4 and aggregates of monocytes and platelets to regula

41 e assessed the potential of peritoneal TLR2, TLR4 and C5a receptors, C5aR and C5L2, as therapeutic ta

42 s increased IL-8 and MCP-1 synthesis through TLR4 and caspase-1.

43 e expression, which, in turn, down-regulates TLR4 and further diminishes TLR4-mediated proinflammator

44 ased pain management via inhibition of glial TLR4 and illustrate the necessity for sex-specific resea

45 These responses are similar to those of TLR4 and MyD88 deficient mice in these models and confir

46 dy, the roles of toll-like receptor (TLR) 2, TLR4 and MyD88, in exacerbation of allergen-induced lung

47 Increased expression of TLR4 and myeloid differentiation protein 2 (MD2) results

48 Therefore, endocytosis of TLR4 and NOX2 into macrophages might be a novel therapeu

49 rate ROS via dynamin-mediated endocytosis of TLR4 and NOX2, independently from MyD88 and TRIF.

50 Non-CSCs express high levels of TLR4 and respond to ligands.

51 cifically addressed the relationship between TLR4 and TLR3.

52 we reveal that the transmembrane domains of TLR4 and TLR6 have an essential role in receptor dimeriz

53 ion, and we demonstrate here that a combined TLR4 and TLR7 adjuvant signals via the appropriate recep

54 that several dose combinations of synthetic TLR4 and TLR7 ligands are potent adjuvants for recombina

55 Combining the TLR4 and TLR7 ligands balances Th1 and Th2-type immune r

56 by this combined adjuvant is dependent upon TLR4 and TLR7 signaling via myeloid differentiation prim

57 ues (RMs) were immunized with NPs containing TLR4 and TLR7/8 agonists mixed with soluble recombinant

58 P (approximately 70 kDa) binds to macrophage-TLR4 and triggers nuclear factor kappa beta activation t

59 C57BL/6 WT, tlr4(-/-) and IL10(-/-) mice were exposed to LPS, and se

60 TLR3 expression was significantly reduced in TLR4(-/-) and Myd88(-/-) mice and following pretreatment

61 Next, we transplanted cardiac MSCs from TLR4(-/-) and WT male mice into the infarcted myocardium

62 8 abolish most TLR (except for TLR3 and some TLR4) and IL-1R signaling in both leukocytes and fibrobl

63 ietic cell deletion of Toll-like receptor 4 (TLR4) and inactivation of the IL-17 axis resulted in alt

64 e identify endothelial Toll-like receptor 4 (TLR4) and the gut microbiome as critical stimulants of C

65 h ligands specific for Toll-like receptor 4 (TLR4) and TLR7/8 encapsulated in poly(lactic-co-glycolic

66 an adaptor protein for Toll-like receptor 4 (TLR4), and thereby impact both virus replication and cel

67 rate that IVH causes a Toll-like receptor 4 (TLR4)- and NF-kappaB-dependent inflammatory response in

68 Hsp90 induce muscle catabolism by activating TLR4, and are responsible for elevation of circulating c

69 These effects were mediated by caspase-11, TLR4, and complement, each of which trigger eicosanoid p

70 tiple receptors, because inhibition of CD36, TLR4, and FcgammaR significantly decreased IL-1beta secr

71 Expression of Toll-like receptor (TLR)2, TLR4, and nuclear factor (NF)-kappa B mRNA levels were a

72 ILC2s expressed TLR1, TLR4, and TLR6, and TLR stimulation induced IL-5 and IL-

73 ssed activation of the FOXO3A pathway, TLR3, TLR4, and TLR7 ligands activated FOXO3A as indicated by

74 The antiproliferative effects of TLR3, TLR4, and TLR7 ligands correlated with significant downr

75 revealed opposing effects of TLR9 and TLR3, TLR4, and TLR7 on the key angiogenic pathways, Fli1 and

76 We demonstrate that ligation of TLR3, TLR4, and TLR9 induces murine DC production of complemen

77 Because TcpB suppresses both TLR4- and caspase-4/11-mediated inflammation, TcpB might

78 Our studies define a TRIF-dependent, TLR4- and type I IFN-independent pathway of sterile live

79 We detected TLR2-, TLR4-, and C5aR-mediated proinflammatory and fibrotic re

80 MyD88-, TRIF-, Toll-like receptor 2 (TLR2)-, TLR4-, and TLR2/4-deficient mice indicated that Acantham

81 us accumbens (NAc), and (3) injection of the TLR4 antagonist (+)-naloxone in mice.

82 r live bacteria enhanced tumorigenesis while TLR4 antagonist CLI095 inhibited it.

83 TLR4 appeared to be essential for the ability of intesti

84 innate immune receptor toll-like receptor 4 (TLR4) as an underlying mechanism mediating these effects

85 ation of cardiac MSCs by LVD was mediated by TLR4, as we found less secretion of inflammatory cytokin

86 Conversely, neutrophil activation through TLR4, as well as through activation by the Gram-negative

87 The high-mobility group box 1 (HMGB1)/TLR4 axis is a key initiator of neuroinflammation follow

88 Activation of TLR4, but not TLR3, induced the expression of miR-718 in

89 Activation of TLR4 by Gram-negative bacteria or lipopolysaccharide acc

90 Activation of TLR4 by lipopolysaccharide (LPS) induces both pro-inflam

91 Stimulation of Toll-like receptor 4 (TLR4) by bacterial lipopolysaccharide (LPS) initiates in

92 Compared with WT cardiac MSCs and saline, TLR4(-/-) cardiac MSCs survived in the cardiac tissue an

93 macologic inhibition and genetic knockout of TLR4 completely abolished ML exosome-induced cytokine pr

94 ibited the formation of the LPS-induced MD-2/TLR4 complex.

95 Indeed, TLR4 conditioned the in vivo mobilization to mesenteric

96 Our data demonstrate that TLR4 conditions induction of oral tolerance to DNFB thro

97 Uninjured IL-1R (-/-) or TLR4 (-/-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7

98 ormed genomic analyses on wild-type (WT) and TLR4(-/-) cultured microglia after sequential exposure t

99 Significantly, TLR4 deficiency preserved the expression of CD47 (don't

100 Further, TLR4 deficiency reduced oxidative stress and increased a

101 TLR4 deficiency was also associated with reduced inflamm

102 and C3H/HeJ (Lps-d) with dysfunctional TLR4 (TLR4 deficiency) were treated without or with Ang-II.

103 In response to Ang-II, TLR4 deficient mice had reduced renal resistive index an

104 ory cytokines from activated cardiac MSCs of TLR4-deficient mice, compared with WT cardiac MSCs.

105 FB gavage was impaired in germ-free mice and TLR4-deficient mice.

106 isease was linked to a Toll-like receptor 4 (TLR4)-dependent mechanism of IAP desialylation with accu

107 sion by activating the Toll-like receptor 4 (TLR4)-dependent pathway via nuclear factor-kappa B (NF-k

108 induced hypersecretion of CSF is mediated by TLR4-dependent activation of the Ste20-type stress kinas

109 chemia/reperfusion-induced pathways for both TLR4-dependent and -independent, IFNAR1-dependent, type

110 way, the LPS-stimulated TLR4 activation and TLR4-dependent cytokine production in human and mouse ce

111 influenza infection, most likely by reducing TLR4-dependent cytokine storm mediated by damage-associa

112 es underwent a rapid catabolic response in a TLR4-dependent manner, including activation of the p38 M

113 pharmacological targets to reduce or reverse TLR4-dependent pain behavior in the rodent.

114 e more sensitive to MNK inhibition than were TLR4-dependent responses.

115 Taken together, our data implicate TLR4-dependent, M1 macrophage trafficking/polarization i

116 erfering with TLR4-TLR6 dimerization using a TLR4-derived peptide, we show that receptor assembly is

117 Mice lacking TLR4 did not exhibit WD-induced myenteric cell loss and

118 Toll-like receptors (TLRs), such as TLR2 and TLR4, dimerize and move laterally across the plasma memb

119 otential scaffold for the development of new TLR4-directed therapeutics.

120 we tested for a gene [Toll-like Receptor 4 (TLR4), encoding the endotoxin receptor]-by-environment i

121 e effects appear to be mediated, in part, by TLR4 expressed on hematopoietic cells, including macroph

122 Bone marrow chimeras revealed that TLR4 expression on hematopoietic cells was necessary for

123 larial protein appears to be a new ligand of TLR4 from W. bancrofti.

124 olymorphisms that increase expression of the TLR4 gene or the gene encoding its co-receptor CD14 are

125 ction for minor allele carrier status at the TLR4 haplotype defined by rs4986790 and rs4986791 (inter

126 d 0.19 were the most prevalent activators of TLR4 in modern wheat and were highly resistant to intest

127 elopment of T/HS-induced ALI and the role of TLR4 in the ML exosome-mediated inflammatory response.

128 Finally, we show that TLR4 in the NAc core is primarily expressed on microglia

129 activation mediated by Toll-like receptor 4 (TLR4) in a glycoprotein (GP)-dependent manner.

130 mediated activation of Toll-like receptor 4 (TLR4) in macrophages results in the coordinated release

131 ed that Lyst specifically controls TLR3- and TLR4-induced endosomal TRIF (TIR domain-containing adapt

132 s through MyD88-dependent, TRIF-independent, TLR4-induced events.

133 ovide new insight into the mechanisms of the TLR4-induced tolerogenic phenotype in human DCs, which c

134 ical blockade of S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induced fibroblast activation.

135 m mediating these effects and establish that TLR4 inhibition in the PAG of females reverses the sex d

136 TLRKO macrophage or macrophage treated with TLR4 inhibitor, indicating that MfP acts through TLR4.

137 inal kinase (JNK) phosphorylation depends on TLR4 initiation.

138 regulation loop involving down-regulation of TLR4, IRAK1, and NF-kappaB.

139 sms of liver fibrosis and also indicate that TLR4 is not entirely critical to LPS-induced acute liver

140 Here, we show that TLR4 is upregulated in KSHV-infected spindle tumor cells

141 Toll-like receptor 4 (TLR4) is a critical component of innate immune signaling

142 IGNIFICANCE STATEMENT: Toll-like receptor 4 (TLR4) is a key mediator of innate immune signaling and h

143 Toll-like receptor 4 (TLR4) is a pattern recognition molecule of the innate im

144 ansformation, KSHV upregulated expression of TLR4, its adaptor MyD88, and coreceptors CD14 and MD2.

145 nol drinking using the following models: (1) Tlr4 knock-out (KO) rats, (2) selective knockdown of Tlr

146 Tlr4 knockdown in mouse NAc did not decrease drinking in

147 Using TLR4 knockout (TLR4.KO) mice, we show that TLR4 plays a

148 -type (WT) and B6.B10ScN-Tlr4(lps-del)/JthJ [TLR4-knockout (KO)] mice.

149 mbinant murine CIRP, but not in the lungs of TLR4 KO mice.

150 and ethanol-trained wild-type (WT), but not Tlr4 KO rats.

151 ed HSC marker) and collagen 1 in both WT and TLR4-KO HSCs.

152 ession of cytokines and chemokines in WT and TLR4-KO HSCs.

153 ic hepatic stellate cells (HSCs) from WT and TLR4-KO mice were assessed in vitro.

154 ession of cytokines and chemokines in WT and TLR4-KO mice.

155 on and injury in previously untreated WT and TLR4-KO mice.

156 aspartate receptors (NMDAR) in the NAc core, TLR4.KO animals exhibit a deficit in low-frequency stimu

157 Consistent with altered NAc LTD, TLR4.KO animals exhibit an attenuation in drug reward le

158 Using TLR4 knockout (TLR4.KO) mice, we show that TLR4 plays a role in NAc syn

159 t TLR4 signaling and hypersensitivity to the TLR4 ligand lipopolysaccharide.

160 er, proliferation of peroxisomes blocked the TLR4 ligand LPS-induced proinflammatory response, as det

161 LPS, a TLR4 ligand, induces macrophages to generate prostagland

162 n with accumulation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosphate.

163 e outcomes, yet endotoxin tolerance-inducing TLR4 ligands are known to protect animals from infection

164 M38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identified a novel

165 ion of TRIM59 was down-regulated by TLR3 and TLR4 ligands in both human and mouse macrophages.

166 Oral biotherapy with TLR4 ligands might be useful to potentiate oral toleranc

167 were significantly up-regulated by TLR3 and TLR4 ligands.

168 In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or nigericin treatment, in

169 Our data show that TLR4 ligation in LPS-primed DCs, induced higher levels o

170 s and confirm that GSTO1-1 is critical for a TLR4-like pro-inflammatory response in vivo.

171 innate immune receptor toll-like receptor 4 (TLR4) localized primarily on microglia.

172 ECs (HDMECs) treated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists showed decreas

173 induction of other proinflammatory genes by TLR4 (LPS), TLR3 (polyriboinosinic-polyribocytidylic aci

174 AM2CSK4, LTA, FSL-1), TLR1/2 (PAM3CSK4), and TLR4 (LPS, MPLA) agonists tested but had almost unimpair

175 liver injury in wild-type (WT) and B6.B10ScN-Tlr4(lps-del)/JthJ [TLR4-knockout (KO)] mice.

176 The results provide evidence of the TLR4/LPS-independent mechanisms of liver fibrosis and al

177 crophage accumulation and expression of p65, TLR4, MCP-1, and osteopontin.

178 4, whereas disulfide HMGB1 and its receptors TLR4/MD-2 and RAGE (receptor for advanced glycation end

179 a direct antagonist effect of calixarenes on TLR4/MD-2 dimerization, pointing at the calixarene moiet

180 TLR4/MD-2 mediates proinflammatory signal delivery follo

181 n factor-2 (MD-2), the coreceptor within the TLR4/MD-2 receptor complex, as the high-affinity sCD83 b

182 LR4-MD2 complex, palmitate binds a monomeric TLR4-MD2 complex that triggers endocytosis, ROS generati

183 rently from LPS-mediated dimerization of the TLR4-MD2 complex, palmitate binds a monomeric TLR4-MD2 c

184 mechanisms, including Toll-like receptor 4 (TLR4)-mediated NADPH oxidase (NOX) activation.

185 ntly demonstrated that Toll-like receptor 4 (TLR4)-mediated neuroinflammation in the periaqueductal g

186 Toll-like receptor 4 (TLR4)-mediated signaling was assessed in primary culture

187 d by tumors, activates toll-like receptor 4 (TLR4)-mediated sterile inflammation.

188 in the lungs can be sustained by persistent TLR4-mediated activation of lung conventional dendritic

189 suppresses Toll-like receptor 2 (TLR2)- and TLR4-mediated innate immune responses by targeted degrad

190 r overt endotoxaemia, synergistically induce TLR4-mediated neurodegeneration and dysmotility.

191 Therefore, we hypothesize that TLR4-mediated opioid tolerance requires TNF signaling.

192 cted in PDE, inhibited PDE-induced, TLR2- or TLR4-mediated profibrotic responses.

193 inding indicates that limiting the excessive TLR4-mediated proinflammatory response in EBOV infection

194 control of toll-like receptor 3 (TLR3)- and TLR4-mediated proinflammatory responses.

195 , down-regulates TLR4 and further diminishes TLR4-mediated proinflammatory signals.

196 mmune) consortium tested the hypothesis that TLR4 mediates excessive ethanol drinking using the follo

197 Here, we show that Toll-like receptor 4 (TLR4) mediates cancer-induced muscle wasting by directly

198 Critically, LLC tumor-bearing TLR4(-/-) mice were spared from muscle wasting due to a

199 loying immunoprecipitation assays, hRETNTg(+)Tlr4(-/-) mice, and human immune cell culture, we demons

200 ha and interleukin-6 (IL-6) was abolished in TLR4(-/-) mice.

201 e mice, Toll-like receptor (TLR) 4 knockout (Tlr4(-/-)) mice, and recombination-activating gene (Rag2

202 WD-fed Toll-like receptor 4 (TLR4)(-/-) mice did not exhibit myenteric cell loss or d

203 tomal feature of H/H-N/N-exposed WT, but not TLR4(-/-), microglia.

204 ck-out (KO) rats, (2) selective knockdown of Tlr4 mRNA in mouse nucleus accumbens (NAc), and (3) inje

205 Functionally, C3H/HeJ (TLR4 mutant) mice reversed M1 macrophage and TH1/TH17 po

206 TLR2-, TLR4-, MyD88-deficient and WT BALB/c mice were intratrac

207 colitis, at least in part, via inhibition of TLR4/MyD88 signaling cascade as well as inactivation of

208 In vitro, baicalein down-regulated the TLR4/MyD88 signaling cascades (NF-kappaB and MAPKs) in l

209 c inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway.

210 ivation is through the toll like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (

211 ore, the role of Toll-like receptor (TLR) 2, TLR4, myeloid differentiation response gene 88, and Toll

212 In the absence of TLR2, TLR4, myeloid differentiation response gene 88, or TRIF,

213 as does treatment with drugs that antagonize TLR4-NF-kappaB signaling or the SPAK-NKCC1 co-transporte

214 ent antioxidant gene expression and inhibits TLR4/NF-kappaB signaling, thus promoting an overall cyto

215 r TLR4, which promotes tumor progression via TLR4/NF-kappaB/STAT3 signaling, providing insights into

216 al to tumorigenesis and metastasis-through a TLR4/nuclear factor kappa-light-chain-enhancer of activa

217 ly activate muscle catabolism via activating TLR4 on muscle cells independent of immune responses.

218 reveal the influence of peritoneal TLR2 and TLR4 on PD-associated fibrosis and describe a therapeuti

219 on microbiota/TLRs and evaluated the role of TLR4 on the tolerogenic function of intestinal dendritic

220 via activation of the toll-like receptor 4 (TLR4) on myeloid cells.

221 zed by and upregulates Toll-like receptor 4 (TLR4) on RAW264.7 macrophages, followed by its endocytos

222 Genetic depletion of TLR4 or SPAK normalizes hyperactive CSF secretion rates

223 Similarly, antibody blockade of TLR2, TLR4, or C5aR differentially inhibited bacteria-induced

224 duction, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spared

225 Additionally, antibodies against TLR2, TLR4, or the coreceptor CD14 reduced the profibrotic res

226 cient for self-renewal, and is suppressed by TLR4 overexpression in CSCs.

227 e results highlight an essential role of the TLR4 pathway and chronic inflammation in KSHV-induced tu

228 Importantly, the TLR4 pathway was activated constitutively in KSHV-transf

229 g TLR4 knockout (TLR4.KO) mice, we show that TLR4 plays a role in NAc synaptic physiology and behavio

230 t binding of S100A9 to Toll-like receptor 4 (TLR4) promotes activation of p38 mitogen-activated prote

231 is silenced in vitro following activation of TLR4 receptor.

232 ated the expression of toll-like receptor 4 (TLR4), receptor for advanced glycation end products (RAG

233 OA synovial fluids (SF) stimulated TLR2 and TLR4 receptors and induced NF-kappaB translocation in TH

234 H/HeJ (Lps-d) mice, deficiency of functional TLR4 reduces oxidative stress and macrophage activation

235 ple laboratories to test the hypothesis that TLR4 regulates excessive alcohol consumption in differen

236 onses, but whether these enzymes function in TLR4 responses of hepatocytes is unknown.

237 ells with lipopolysaccharide, the ligand for TLR4, results in SYK activation and that this is depende

238 en recognition receptors (PRRs) (i.e., TLR3; TLR4), revealing a stimulus-selective role for TBK1 in m

239 We further demonstrate that inhibition of TLR4 signaling abolishes EBOV GP-mediated NF-kappaB acti

240 ciency caused hyperresponsive TRAM-dependent TLR4 signaling and hypersensitivity to the TLR4 ligand l

241 We propose a role for miR-718 in controlling TLR4 signaling and inflammatory cytokine signaling throu

242 However, altering TLR4 signaling can attenuate the proinflammatory cascade

243 of TLR3 up-regulation that is induced by LPS-TLR4 signaling in a dose- and time-dependent manner in A

244 TLR4 signaling in hepatic macrophages is increased after

245 We found that Nox4 mediated LPS-TLR4 signaling in hepatocytes via NF-kB and AP-1 pathway

246 ore, our data suggest that Nox4 mediates LPS-TLR4 signaling in human hepatoma cells and murine hepato

247 ameliorated ethanol-induced sensitization of TLR4 signaling in macrophages/monocytes, suggesting that

248 ggest that in human monocytes, both TLR2 and TLR4 signaling induce pro-IL-1beta expression, but the m

249 ed the involvement of Lyn tyrosine kinase in TLR4 signaling of macrophages, distinguishing its cataly

250 DC maturation and cytokine secretion through TLR4 signaling pathway.

251 The effect of HDE required TLR4 signaling predominantly in lung hematopoietic cells

252 microRNAs to identify negative regulators of TLR4 signaling reciprocally modulated by ethanol and HA3

253 TLR4 signaling suppresses CSC properties by reducing ret

254 serves as an intrinsic negative regulator of TLR4 signaling that targets TIRAP.

255 TLR4 signaling was increased in Kupffer cells by ethanol

256 oreover, guanidinocalixarenes also inhibited TLR4 signaling when TLR4 was activated by a non-LPS stim

257 Here, we show that Ezrin links CFTR and TLR4 signaling, and is necessary for PI3K/AKT signaling

258 CD14/MD-2 ligands and therefore modulate the TLR4 signaling, we present here a panel of amphiphilic g

259 tein TcpB that negatively regulates TLR2 and TLR4 signaling.

260 ein (GP), which can be inhibited by blocking TLR4 signaling.

261 al adaptive immune system and independent of TLR4 signaling.

262 ereby determining the negative regulation of TLR4 signaling.

263 c sized hyaluronic acid 35 (HA35) normalizes TLR4 signaling; however, the mechanisms for HA35 action

264 Thus, therapeutic control of the TLR4 signalling pathway is of major interest.

265 on, and genetic or pharmacologic blockade of TLR4 signalling prevents CCM formation in mice.

266 TLR4 signalling through the MyD88 and TRIF-dependent pat

267 Our results demonstrate that TLR4 signals through two distinct pathways, one via the

268 n 3 (STAT3) signaling pathway and negated by TLR4-specific antibody and antagonist.

269 or restored Tollip expression and normalized TLR4-stimulated TNFalpha expression.

270 't eat me signal) on cardiac MSCs after both TLR4 stimulation in vitro and transplantation into the i

271 TLR4 stimulation with lipopolysaccharides or live bacter

272 FP7 selectively blocked TLR4 stimulation, but not TLR1/2, TLR2/6, or TLR3 activa

273 Upon stimulation of TLR4, the rapid induction of IFN-beta was inhibited in c

274 binds the LPS receptor Toll-like receptor 4 (TLR4) through its N terminal and modulates STAT3 and TBK

275 hepatic inflammatory markers (F4/80, MCP-1, TLR4, TLR2 and IL-1beta) and effector caspase (caspase 3

276 TLR-4 and C3H/HeJ (Lps-d) with dysfunctional TLR4 (TLR4 deficiency) were treated without or with Ang-

277 These data show complex roles for TLR4, TLR5, IL-1R and CD11c+ cells in constitutive epith

278 ew complex composed of Toll-like receptor 4 (TLR4), TLR6, and CD36 induced by fibrillary Abeta peptid

279 Moreover, we shed new light on TLR4-TLR6 assembly and localization and show the potenti

280 Inhibition of TLR4-TLR6 assembly was associated with reduced secretion

281 ization and show the potential of inhibiting TLR4-TLR6 dimerization as a treatment of Alzheimer's dis

282 Our findings support TLR4-TLR6 dimerization induced by Abeta.

283 By interfering with TLR4-TLR6 dimerization using a TLR4-derived peptide, we

284 However, the assembly site of TLR4-TLR6-CD36 and the domains participating in Abeta-in

285 d binding to their extracellular domain, the TLR4-TLR6-CD36 complex assembly has been suggested to be

286 ls responded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and to IL-1

287 a triple adjuvant combination, TLR4/TLR9 and TLR4/TLR7/TLR9, for further evaluation and found that bo

288 patients displayed dysregulated responses to TLR4, TLR8, and TLR7 stimulation.

289 ed a dual and a triple adjuvant combination, TLR4/TLR9 and TLR4/TLR7/TLR9, for further evaluation and

290 n, initiates secretion of MRP8/14 that binds TLR4 to elicit the extension of beta2-integrin to an int

291 acteria that activates Toll-like receptor 4 (TLR4) to trigger proinflammatory responses.

292 lixarenes also inhibited TLR4 signaling when TLR4 was activated by a non-LPS stimulus, the plant lect

293 Furthermore, TLR2 but not TLR4 was critical for sensing of cell wall extracts and

294 KSHV induction of TLR4 was mediated by multiple viral miRNAs.

295 Although TLR4 was not a critical determinant of excessive drinkin

296 Binding of MfP to Toll-like receptor 4 (TLR4) was determined by co-immunoprecipitation, fluoresc

297 Very little activity was seen downstream of TLR4, which can also activate an MyD88-independent pathw

298 a clinically relevant endogenous ligand for TLR4, which promotes tumor progression via TLR4/NF-kappa

299 Blockade of morphine binding to PAG TLR4 with (+)-naloxone potentiated morphine antinocicept

300 ia in vitro demonstrated that stimulation of TLR4 with lipopolysaccharide, widely used to examine mic