ライフサイエンスコーパス: TLR3

1 nocytes that activates Toll-like receptor 3 (TLR3).

2 n recognition receptor Toll-like receptor 3 (TLR3).

3 ntaining protein TRIF is the sole adaptor of TLR3.

4 UVB damage is dependent on the activation of TLR3.

5 usively on RIG-I and independent of MDA5 and TLR3.

6 ry viruses and triggers immune responses via TLR3.

7 cacy is due to a higher binding of endosomal TLR3.

8 risk alleles for CFH, ARMS 2, HTRA1, C3, or TLR3.

9 r 4 (TLR4), but not TRIF-dependent poly(I:C)/TLR3.

10 nt receptors, including the TNF receptor and TLR3.

11 g stimulation through TLR2 and TLR4, but not TLR3.

12 I:C) co-localization to endosomes containing TLR3.

13 signaling to double-stranded RNA (dsRNA) by TLR3.

14 cytidylic acid (poly(I:C)) bind and activate TLR3.

15 strating surface expression of both forms of TLR3.

16 addressed the relationship between TLR4 and TLR3.

17 We detected 2 rare missense mutations in TLR3: 1 in a patient with HSE (p.Leu297Val) and 1 in a p

18 or the activation of murine female cDCs upon TLR3, -4, -7, and -9 stimulation.

19 co-infection in vitro and suppression of the TLR3,4/NF-kappaB/TNF-alpha pathway as an important under

20 d p-IkappaBalpha expression, suggesting that TLR3,4/NF-kappaB/TNF-alpha pathway play an important rol

21 uated the effect of Matrine on virus-induced TLR3,4/NF-kappaB/TNF-alpha pathway.

22 LPS induction of messenger RNAs encoding the TLR3/4 signaling adaptor protein Pellino-1 and the trans

23 es but are not required for amplification of TLR3/4-induced CXCL1 expression.

24 inflammatory cytokine secretion but enhanced TLR3/4-triggered IFN-beta production via binding to and

25 ein kinase 4 (STK4) differentially regulates TLR3/4/9-mediated inflammatory responses in macrophages

26 protein kinase 1, a kinase also linked with TLR3/4/TRIF signaling, is required and involves a stress

27 tic background that are triple-deficient for TLR3, -7, and -9 (Tlr3/7/9(-/-)) are highly susceptible

28 autophagy because macrophages deficient for TLR3, -7, and 9, UNC93B1, or MyD88 failed to undergo L.

29 Tlr3/7/9(-/-) mice are as susceptible as mice deficient

30 the ears of Leishmania-infected C57BL/6 and Tlr3/7/9(-/-) mice, indicating that autophagy operates d

31 t are triple-deficient for TLR3, -7, and -9 (Tlr3/7/9(-/-)) are highly susceptible to L. major infect

32 We also confirmed that Myd88(-/-), Tlr3/7/9(-/-), and Unc93b1(-/-) cells were highly permis

33 Toll-like receptor-3 (TLR3), a member of the pathogen recognition receptor fam

34 Moreover, variations in human TLR3, a potent inducer of IFNs, were proposed to underli

35 All TLRs except TLR3 achieve these outcomes by using the signaling adapt

36 esponses attributed to toll-like receptor 3 (TLR3)-activated Kupffer and liver sinusoidal endothelial

37 duced SHP-1 protein, and acts selectively on TLR3-activated JNK2.

38 We showed that supernatant from TLR3-activated macrophage cultures could efficiently inh

39 Further analyses demonstrated that TLR3-activated macrophages release exosomes that contain

40 pro-inflammatory mediators by MSCs, whereas TLR3-activated MSCs displayed a milder pro-inflammatory

41 Recognition of viral dsRNA by endosomal TLR3 activates innate immune response during virus infec

42 y analysis of gene expression changes during TLR3 activation highlighted 41 genes also related to neu

43 s issue of Cancer Cell, Liu et al. show that TLR3 activation in lung epithelial cells by tumor exosom

44 gs demonstrate the potential of BTV-mediated TLR3 activation in macrophage innate immunity against HI

45 TLR3 activation in the skin induces inflammation and inc

46 In this paper we investigated the effect of TLR3 activation on a Marek's disease lymphoma-derived ch

47 TLR3 activation promotes expression of hair follicle ste

48 t that expression of vIRF1 in the context of TLR3 activation results in decreased ISG15 conjugation o

49 emonstrated that S100A9 functions during pre-TLR3 activation stages by facilitating maturation of TLR

50 Recently, TLR3 activation was also shown to aid wound repair and i

51 ndings identify a link between ZIKV-mediated TLR3 activation, perturbed cell fate, and a reduction in

52 TLR4 stimulation, but not TLR1/2, TLR2/6, or TLR3 activation.

53 impairs type I IFN production in response to TLR3 activation.

54 RC5, in the context of Toll-like receptor 3 (TLR3) activation and IFN induction.

55 TLR3-activation thus establishes a type I IFN-dependent

56 pendent cytokine production by promoting the TLR3 adaptor protein TRIF-assembled signalling complex.

57 The TLR3 agonist poly (I:C) activated TLR3 pathway and inhib

58 agonists of TLR2 (Pam3Cys), TLR4 (LPS), and TLR3 agonist Poly(I:C).

59 mAbs were administered systemically with the TLR3 agonist polyinosinic:polycytidylic acid or were giv

60 acid (polyIC; a dsRNA mimetic that acts as a TLR3 agonist).

61 olyadenylic-polyuridylic acid (poly(A:U)), a TLR3 agonist, and R848 (resiquimod), a TLR7 agonist, in

62 ctory to maturation after stimulation with a TLR3 agonist, demonstrating that this tolerized state is

63 nistration of an ISCOMATRIX vaccine with the TLR3 agonist, polyinosinic-polycytidylic acid, and TLR9

64 nistic CD40 antibody, soluble antigen, and a TLR3 agonist, referred to as CoAT.

65 ay in vivo with LPS or Toll-like receptor-3 (TLR3) agonist resulted in high mortality in wild-type mi

66 ic acid (poly(I:C)), a Toll-like receptor 3 (TLR3) agonist used as a mimetic to study viral infection

67 Our findings suggest evaluation of TLR3 agonists in drug therapy.

68 s imply that metastatic IECs express surface TLR3, allowing it to sense extracellular stimuli that tr

69 described for the first time that synergy of TLR3 and 7 ligands could significantly enhance the funct

70 oping a Rab8a activation assay, we show that TLR3 and 9 agonists also activate Rab8a.

71 Knocking down dsRNA sensors TLR3 and MAVS reduces this response 2-fold and blocking

72 he RIP-B7.1 model is critically dependent on TLR3 and MyD88 pathways, and involves modulation of the

73 nt of hepatocytes alone had little effect on TLR3 and RIG-I signaling pathways, EGCG significantly en

74 ly regulated CXCL10 induction in response to TLR3 and RIG-I stimuli, while only C/EBP-beta negatively

75 etic dsRNA that acts as an immune agonist of TLR3 and RLR to activate dendritic and natural killer ce

76 IRAK-4 or MyD88 abolish most TLR (except for TLR3 and some TLR4) and IL-1R signaling in both leukocyt

77 eceptors, we demonstrate the crucial role of TLR3 and Src in in-poly(I:C)-induced apoptosis.

78 ntracellular microbial nucleic acid sensors, TLR3 and STING, recognize pathogen molecules and signal

79 ivity in epithelial cells via stimulation of TLR3 and suggest a novel mechanism by which influenza in

80 helial cells (IECs), metastatic IECs express TLR3 and that TLR3 promotes invasiveness of these cells.

81 IFN-beta promoter stimulator 1, adaptors for TLR3 and the RLRs, respectively.

82 TLR3 and TLR2/6 ligands led to a rapid increase in LLT1

83 < 0.01) greater in TR APOE4/4 microglia with TLR3 and TLR4 activators.

84 Responses through TLR3 and TLR4 exhibited the greatest sensitivity, reflec

85 2 and TRIM38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identifie

86 e expression of TRIM59 was down-regulated by TLR3 and TLR4 ligands in both human and mouse macrophage

87 61) that were significantly up-regulated by TLR3 and TLR4 ligands.

88 rget gene expression upon engagement of both TLR3 and TLR4 pathways, as well as in H1N1-infected macr

89 iched accessory protein that is important in TLR3 and TLR4 signaling.

90 Signaling through TLR3 and TLR4, which lie upstream of IRF3, induced insul

91 Reduced TLR3 and TLR7 expression and TLR downstream-signaling mo

92 Coactivation of the TLR3 and TLR7 pathways synchronizes the interaction of I

93 f CD83, CD86, and MHC class I in response to TLR3 and TLR7/8-agonists.

94 ISCOMATRIX vaccines combined with TLR3 and TLR9 agonists represent a promising cancer immu

95 TLR3 and TLR9 expression and downstream MYD88 signalling

96 The nucleic acid recognizing endosomal TLRs, TLR3 and TLR9, had a potent ability to induce CD8 T cell

97 ckout virus was less effective at inhibiting TLR3 and TRL4 signaling and displayed lower infectivity.

98 t Sendai and vesicular stomatitis virus in a TLR3 and type I IFN receptor-dependent manner.

99 cular, dsRNA receptors Toll-like receptor 3 (TLR3) and cytosolic helicases expressed by cancer cells,

100 ctivation of endosomal Toll-like receptor 3 (TLR3) and downstream innate immune signaling.

101 amaged skin, activates Toll-Like Receptor 3 (TLR3) and its downstream effectors IL-6 and STAT3 to pro

102 ich are devoid of TLR (with the exception of TLR3) and RIG-I-like helicase signaling, whereas in vacc

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

104 Genetic deletion of TLR7 or MyD88, but not TLR3, and inhibition of the MAPKs (JNK and p38) or NF-ka

105 homozygous for targeted disruption of TLR9, TLR3, and myeloid differentiation factor-88 (MyD88), and

106 ling, including responses triggered by TLR4, TLR3, and TLR2 activation, and it is enhanced by IFN-gam

107 Toll-like receptor (TLR)1/2, TLR3, and TLR4 agonists all induced the cells to retain

108 In sharp contrast, TLR3- and MyD88-deficient mice were protected from diabe

109 We found that TLR3- and STAT1-deficient cardiomyocytes were not more s

110 sis revealed that Lyst specifically controls TLR3- and TLR4-induced endosomal TRIF (TIR domain-contai

111 HTLV-1 infection of monocytes inhibited TLR3- and TLR4-induced ISG expression by 50 to 90% depen

112 ase 3 (RIPK3), an essential factor for TNF-, TLR3-, and TLR4-induced necroptosis.

113 docytosis, and could be blocked with an anti-TLR3 antibody, indicating that TLR3 can still signal fro

114 ceptors in metabolic disorders and implicate TLR3 as a key control system in metabolic regulation.

115 nal interaction between LUBAC components and TLR3 as crucial for immunity to influenza A virus infect

116 ces phosphorylation of Toll-like receptor 3 (TLR3) at tyrosine 759 and subsequently triggers signalin

117 suggested an essential role of the iNOS/Src/TLR3 axis in IFN-beta production in macrophages.

118 Here we show that TLR3 binding to dsRNA promotes post-translational inflam

119 pe lectin-like receptor 9A, XCR1, CADM1, and TLR3 but lack TLR4 and TLR9.

120 l-like receptor 4 (TLR4) and by poly(I.C) of TLR3 but not of TLR7/8 with imiquimod.

121 Ectopic expression of wild type TLR3, but not its 759-phenylalanine mutant, restored Src

122 TLR4 and TLR3 can both use the Toll-IL-1 receptor domain-containi

123 with an anti-TLR3 antibody, indicating that TLR3 can still signal from the cell surface of these cel

124 uine (IC50 11.9 mum) and a dominant negative TLR3 construct (pZERO-hTLR3).

125 unction of Toll-like receptors (TLRs) except TLR3, contained VH4-34-expressing clones and showed decr

126 S100A9 was required for maturation of TLR3 containing early endosome (EE) into LE, the compart

127 3 interaction was critical for maturation of TLR3 containing EE into LE because TLR3 could not be det

128 ivation stages by facilitating maturation of TLR3 containing EE into LE.

129 ration of TLR3 containing EE into LE because TLR3 could not be detected in the LE of polyIC-treated S

130 TLR3 deficiency also modified the plasma lipid profile,

131 Conversely, TLR3-deficient animals fail to initiate WIHN.

132 g a diet-induced obesity model, we show that TLR3-deficient mice had enhanced glycemic control, facil

133 IECs contained both full-length and cleaved TLR3, demonstrating surface expression of both forms of

134 ibition of BRD4 blocks Toll-like receptor 3 (TLR3)-dependent neutrophilia and RSV-induced inflammatio

135 For instance, PAR1 positively regulates TLR3-dependent expression of the antiviral protein inter

136 androgen-dependent PCa cell line LNCaP in a TLR3-dependent fashion, whereas only a weak apoptotic ef

137 e of HBsAg, hepatic HBV replication leads to Tlr3-dependent interferon responses in non-parenchymal l

138 t junctions, and that the ncRNA U1 acts in a TLR3-dependent manner to induce expression of skin barri

139 patterns, which results in activation of the TLR3-dependent signaling cascade.

140 TRIF-mediated signaling pathways of TLR4 and TLR3 discovered here could have a major impact in the de

141 act TAR molecule was able to bind to PKR and TLR3 effectively, whereas the 5' and 3' stems (TAR micro

142 a missense single nucleotide polymorphism in TLR3 (encoding L412F) was linked to elevated insulin lev

143 TLR3 engagement in CD8(+) DCs promotes cross-presentatio

144 d that these antiviral genes were induced by TLR3 engagement in primary CD8(+) DCs, and indicated tha

145 hinitis patients and a parallel reduction in TLR3 expression and increased RV-16 replication compared

146 We conclude that altered TLR3 expression and localization may have implications f

147 IL-4 and IL-13, through inhibition of TLR3 expression and signalling (IRF3), impair immune res

148 ncreased rhinovirus replication and impaired TLR3 expression in bronchial epithelial cells.

149 Phi from C57BL/6 mice, while the LPS-induced TLR3 expression was significantly reduced in TLR4(-/-) a

150 We also provide evidence that TLR3-facilitated antiviral signaling predates the origin

151 Subsequently, TLR3 failed to colocalize with its agonist (i.e., biotin

152 olocalization and interaction of S100A9 with TLR3 following polyIC treatment.

153 r virus encephalitis and support the role of TLR3 genetic defects as risk factors for HSE in adults.

154 Surprisingly, genetic deletion of TLR3 had no impact on the RNA-induced MIP-2 response.

155 However it is unclear whether TLR3 has same function against chicken lymphoma.

156 We tested the role of TLR3-IFN immunity using human induced pluripotent stem c

157 is is the first report about the function of TLR3 in chicken T-cell lymphoma, especially in signal pa

158 We examined the function of TLR3 in glucose metabolism and type 2 diabetes-related p

159 that the synergistic effect between TLR4 and TLR3 in macrophages is an important determinant in acute

160 We confirm the involvement of TLR3 in this process using chloroquine (IC50 11.9 mum) a

161 t (poly I:C) to target Toll-like receptor 3 (TLR3) in endosomes.

162 Activation of TLR4, but not TLR3, induced the expression of miR-718 in macrophages.

163 we performed a comprehensive analysis of the TLR3-induced antiviral program and cell-autonomous immun

164 However, TLR3-induced CXCL10 was triggered by immobilized poly(I:

165 eases formation of a previously unrecognized TLR3-induced death-inducing SC, leading to enhanced cell

166 Specifically, TLR3-induced ISG15 conjugation and protein levels of cel

167 wer levels of SHP-1, which normally inhibits TLR3-induced JNK2 phosphorylation, thereby increasing in

168 f human organoids and mouse neurospheres and TLR3 inhibition reduced the phenotypic effects of ZIKV i

169 S100A9-TLR3 interaction was critical for maturation of TLR3 con

170 ts of Th2 cytokines on Toll-like receptor 3 (TLR3), interferon-responsive factor 3 (IRF3) and nuclear

171 High expression of the dsRNA sensor TLR3 is a distinctive feature of these cross-presenting

172 lusion that recognition of endogenous RNA by TLR3 is an important step in the program of skin barrier

173 TLR3 is highly expressed in the pancreas, suggesting tha

174 with dsRNA to affect signal transduction by TLR3 is not completely understood.

175 3 and the molecule UNC93B1, indicating that TLR3 is required for recognizing poly A:U.

176 that TRIF, a critical adaptor downstream of TLR3, is targeted by EV68.

177 tion as well as exocytotic protein VAMP-2 in Tlr3(-/-) islets.

178 TLR3 knockdown destabilized Src and reduced the nuclear

179 hypothesized that influenza would stimulate TLR3 leading to activation of latent TGFbeta via alphavb

180 d by pattern-recognition receptors (TLR9 and TLR3) leading to a type-I IFN mediated innate immune res

181 e that sensing of HCV infection by RIG-I and TLR3 leads to direct recruitment of NF-kappaB and IRF3 t

182 The TLR3 ligand [poly(I:C)] markedly suppressed VEGF secreti

183 lls (MoDCs) were treated with poly (I: C) of TLR3 ligand and imiquimod of TLR7 ligand, along with ina

184 vers that recruit leukocytes to TME, such as TLR3 ligand in B16 tumors, greatly enhanced nutlin-induc

185 ssion of skin barrier repair genes, that the TLR3 ligand Poly (I:C) also induced expression and funct

186 K3beta physically associates with TRAF6 in a TLR3 ligand poly I:C-dependent manner.

187 n agonistic anti-CD40Ab, with or without the TLR3 ligand poly IC:LC.

188 tion and nephritis following exposure to the TLR3 ligand poly(I:C).

189 The TLR3 ligand poly(inosinic-cytidylic) acid was applied in

190 In this study, we assessed the effect of the TLR3 ligand polyinosinic-polycytidylic acid (poly IC) on

191 the presence of stimulating anti-CD40 Ab and TLR3 ligand polyinosinic-polycytidylic acid induces prot

192 quential challenges with LPS and Poly I:C, a TLR3 ligand, which was physiologically associated with a

193 We found that TLR3-ligand polyinosinic-polycytidylic acid and human rh

194 We found that TLR3 ligands induced the strongest release of both proin

195 Taken together, our findings indicate that TLR3 ligands polarize the inflammatory phenotype of MSCs

196 Notably, TLR3 ligands triggered a biphasic cytokine response, wit

197 or environmental stimuli (cigarette smoke or TLR3 ligands) implicated in COPD pathogenesis.

198 gs to CD8(+) T cells and respond strongly to TLR3 ligands.

199 , which subsequently enhanced sensitivity to TLR3 ligation and amplified the production of IL-6 and I

200 Our findings indicate that mucosal TLR3 ligation may be used to improve CD8 T cell response

201 Our results therefore show that dsRNA and TLR3 link the earliest events of mammalian skin wounding

202 Importantly, TLR3-LXR signal crosstalk promotes recruitment of NCOA5

203 beta, which likely in turn induces increased TLR3, MDA5, and RIG-I proteins.

204 In contrast to direct TLR3/mda5 signaling, IFNs are required for upregulation

205 agonists of the virus-recognizing receptors TLR3/MDA5, TLR7/-8, and TLR9 and found that this treatme

206 The mechanisms underlying TLR3-mediated apoptosis may contribute to the developmen

207 Intriguingly, excessive TLR3-mediated cell death, induced by double-stranded RNA

208 In contrast, TLR3-mediated DC maturation was completely dependent on

209 LR3-signaling complex (SC), thereby enabling TLR3-mediated gene activation.

210 hat the antimicrobial protein REG3A controls TLR3-mediated inflammation after skin injury.

211 Here we report that EV68 inhibits TLR3-mediated innate immune responses by targeting TRIF.

212 Thus, LUBAC components control TLR3-mediated innate immunity, thereby preventing develo

213 reening of a small-molecule library based on TLR3-mediated NF-kappaB activation.

214 aling but were independent of the MyD88- and TLR3-mediated pathways.

215 acts with TRAF6 and positively regulates the TLR3-mediated signalling.

216 Despite having high insulin levels, Tlr3(-/-) mice did not experience disturbances in whole-

217 s were shown to have functional relevance as Tlr3-/- mice displayed a delay in skin barrier repair fo

218 ata herein expand the phenotypic spectrum of TLR3 mutations to varicella-zoster virus encephalitis an

219 Cells expressing NS3/4A and TLR3/MyD88/IFN-beta promoter stimulator 1(-/-) mouse emb

220 t of the overexpressed ISGs, including GBP1, TLR3, OAS1, EIF2AK2, HLA-E, IFI6, and STAT1, showed high

221 Tumors lacking Tlr3 or Ifnar failed to respond to chemotherapy unless t

222 ot possess signaling capacity independent of TLR3 or the RLRs.

223 inhibit IFN-alpha/beta production induced by TLR3 or TLR4 agonists, this occurs in a dsRNA-independen

224 production induced by Toll-like receptor 3 (TLR3) or TLR4 agonists but failed to inhibit proinflamma

225 mmatory cytokine production induced by TLR2, TLR3, or TLR4 agonists.

226 significant enrichment of rare variations in TLR3- or IFN-alpha/beta-related genes.

227 a TLR7 antagonist, but remained the same in TLR3- or Trif-deficient cells.

228 The TLR3 agonist poly (I:C) activated TLR3 pathway and inhibited tumor cells proliferation thr

229 y spared the polyinosinic-polycytidylic acid/TLR3 pathway.

230 e I IFN production in astrocytes through the TLR3 pathway.

231 efects in genes of the Toll-like receptor 3 (TLR3) pathway are associated with susceptibility to herp

232 ein 5 (RIG-I/MDA5) and Toll-like receptor 3 (TLR3) pathways.

233 TLR3 plays a crucial, albeit controversial, role in vira

234 rmal microvascular ECs (HDMECs) treated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agoni

235 f other proinflammatory genes by TLR4 (LPS), TLR3 (polyriboinosinic-polyribocytidylic acid), TLR2 (Pa

236 promoted the binding of IRF1 and IRF2 to the Tlr3 promoter, without which inflammatory cytokine and t

237 IECs), metastatic IECs express TLR3 and that TLR3 promotes invasiveness of these cells.

238 For all TLRs except TLR3, recruitment of the adapter, myeloid differentiatio

239 aling of nonself dsRNA through both MDA5 and TLR3 remains intact in IBV-infected cells.

240 ic acid and poly(I:C) signaling via TLR2 and TLR3, respectively, was significantly reduced.

241 ) DCs, and indicated that many are secondary TLR3-response genes requiring autocrine IFN-beta stimula

242 it is poorly understood how TRAF6 regulates TLR3 responses.

243 inefficient RIG-I and Toll-like receptor 3 (TLR3) responses.

244 By using a TLR3-restricted double-stranded RNA agonist, rintatolimo

245 uced the expression of Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I (RIG-I) and severa

246 sRNAs-induced the expression of IFN-lambda1, TLR3, RIG-I and antiviral ISGs in hepatocytes.

247 TLR3 rs3775296-T was associated with photosensitivity (p

248 ion of LL-37, inhibited LL-37 enhancement of TLR3 signal transduction.

249 ified intracellular S100A9 as a regulator of TLR3 signaling and demonstrated that S100A9 functions du

250 We identify a pivotal role of LUBAC in TLR3 signaling and discover a functional interaction bet

251 , DOK3 plays a critical and positive role in TLR3 signaling by enabling TRAF3/TBK1 complex formation

252 of poly IC was dependent on amplification of TLR3 signaling by nonhematopoietic radioresistant cells

253 We found a role for TRIL in both TLR4 and TLR3 signaling in mixed glial cells, consistent with the

254 Furthermore, TLR3 signaling of macrophages by BTV16 resulted in the i

255 xcessive inflammation by blocking downstream TLR3 signaling.

256 ify LUBAC components as interacting with the TLR3-signaling complex (SC), thereby enabling TLR3-media

257 in PC3 and DU145 cells: one mediated by the TLR3/Src/STAT1 axis, leading to apoptosis, and the other

258 On the other hand, TLR3 stimulation strongly increases leukocytes affinity

259 n XCR1(+) mDC had much stronger responses to TLR3 stimulation than other myeloid cells.

260 posure to poly(I.C) (a Toll-like receptor 3 [TLR3] stimulus) and 5' poly(U) HCV RNA (a retinoic acid-

261 ory skin phenotype, as genetic coablation of Tlr3 substantially ameliorated cpdm dermatitis.

262 igger type I IFN production by DCs that lack TLR3, such as plasmacytoid DCs or CD8(-) DCs.

263 and Il12b via IFN regulatory factor (IRF)1 (TLR3-TIR domain-containing adaptor inducing IFN-beta [TR

264 neumophila in C57BL/6 MyD88(-/-), TLR2(-/-), TLR3(-/-), TLR4(-/-), TLR9(-/-), IL-1R(-/-), and IL-18(-

265 gnificantly down-regulated the expression of TLR3, TLR4 and TNF-alpha although it, to some extent, su

266 This applies to toll-like receptors 3 and 4 (TLR3, TLR4), which sense double-stranded RNA and high-mo

267 atients who bear loss-of-function alleles in TLR3, TLR4, and FPR1 exhibit a reduced metastasis-free a

268 suppressed activation of the FOXO3A pathway, TLR3, TLR4, and TLR7 ligands activated FOXO3A as indicat

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

270 s work revealed opposing effects of TLR9 and TLR3, TLR4, and TLR7 on the key angiogenic pathways, Fli

271 We demonstrate that ligation of TLR3, TLR4, and TLR9 induces murine DC production of com

272 rophils lacking Toll-like receptor-2 (TLR2), TLR3, TLR4, TLR7 and TLR9, which are normally less stron

273 icantly downmodulated the response of TLR2-, TLR3-, TLR4-, and TLR9-expressing HEK293 cells to stimul

274 pathogen recognition receptors (PRRs) (i.e., TLR3; TLR4), revealing a stimulus-selective role for TBK

275 Six SNPs of TLR3, TLR7, and TLR8 were genotyped to determine their a

276 y intracellular PRRs such as endosomal TLRs (TLR3, TLR7, TLR8, and TLR9) and cytoplasmic proteins (ab

277 antagonizing endosomal toll-like receptors (TLR3, TLR7/8, and TLR9), proteins involved in innate imm

278 We show that in CD4(+) T cells, NA-TLRs, TLR3, TLR8, and TLR9 are upregulated by FcgammaRIIIa-pSy

279 Trafficking of TLR3 to the endolysosomal compartment arising from fusio

280 echanism(s) and cellular factor(s) governing TLR3 trafficking is limited.

281 ar S100A9 protein as a critical regulator of TLR3 trafficking.

282 n-activated protein kinases by the TLR4- and TLR3-TRIF axes determined the type I IFN dependency for

283 IECs also induced the chemokine CXCL10 in a TLR3-, TRIF-, and IRF3-dependent manner but failed to pr

284 (I:C) stimulated IFN-beta mainly through the TLR3/TRIF pathway and IL-8 through an unidentified pathw

285 proved to be dependent on CD11c(+) cells and TLR3/TRIF signaling.

286 imed at clarifying the mechanisms underlying TLR3 triggered exacerbation of experimental allergic ast

287 Interestingly, Src phosphorylated TLR3 Tyr-759 in vitro and in vivo.

288 ound that dsRNA stimulation induces biphasic TLR3 Tyr-759 phosphorylation in macrophages.

289 , via down-regulation of Src, dsRNA-elicited TLR3 Tyr-759 phosphorylation, the nuclear accumulation o

290 In addition to the immediate TLR3 Tyr-759 phosphorylation, we identified a second wav

291 The enhanced TLR3 up-regulation in AMPhi augmented the expression of

292 cute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4-MyD88-NF-kappaB

293 We explored a novel mechanism of TLR3 up-regulation that is induced by LPS-TLR4 signaling

294 All TLRs, with the exception of TLR3, use an MyD88 adapter to Toll/IL-1 to initiate a pr

295 TLR3 uses the toll receptor 3/4 induction factor adapter

296 innate immune receptor Toll-like-Receptor 3 (TLR3) was upregulated after ZIKV infection of human orga

297 Influenza stimulates toll-like receptor 3 (TLR3), which can increase RhoA activity, a key event pri

298 lated genes, including Toll-like receptor 3 (Tlr3), which encodes an innate immune sensor of viral do

299 arly relevant for viruses detected mainly by TLR3, which may not trigger type I IFN production by DCs

300 However, activation of TLR3 with exogenous ligands indicated additional HBs-ind