ライフサイエンスコーパス: TLR3

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

2 RNA (siRNA) were used to confirm the role of TLR3.

3 nt receptors, including the TNF receptor and TLR3.

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

5 strating surface expression of both forms of TLR3.

6 addressed the relationship between TLR4 and TLR3.

7 ntaining protein TRIF is the sole adaptor of TLR3.

8 UVB damage is dependent on the activation of TLR3.

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

10 ry viruses and triggers immune responses via TLR3.

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

12 SLIT2 by acting on the RNA-sensing receptor TLR3.

13 responses via the dsRNA sensors, RIG-I, and TLR3.

14 demonstrating robust expression of TLR2 and TLR3.

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

16 terozygous genotypes of the TLR2 2029C/T and TLR3 1377C/T and -7C/A SNPs may serve as genetic biomark

17 the presence of TLR2 (2029C/T and 2258G/A), TLR3 (1377C/T, 1234C/T, and -7C/A), TLR4 (896A/G, 1196C/

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

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

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

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

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

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

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

30 The wild-type genotype of the TLR3 -7C/A SNP was associated with a 3-fold increased ri

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

32 (hPDL cells) express several TLRs, including TLR3, a nucleotide sensing receptor that recognizes doub

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

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

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

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

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

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

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

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

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

42 TLR3 activation promotes expression of hair follicle ste

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

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

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

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

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

48 e not propagated following HIV infection and TLR3 activation.

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

50 re treated with various doses of poly I:C, a TLR3 activator.

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

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

53 Exposure of PBECs to concomitant TLR3 agonist poly(I:C) and HDM resulted in a significant

54 imaging and radiotherapy, and linkage of the TLR3 agonist poly(I:C) as a model immune-oncologic agent

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

56 ic hypoxia/SU5416 rats were treated with the TLR3 agonist polyinosinic/polycytidylic acid (Poly[I:C])

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

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

59 (ISV), combining Flt3L, radiotherapy, and a TLR3 agonist, which recruited, antigen-loaded and activa

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

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

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

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

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

65 o decipher the relative contributions of the TLR3 and cGAS-STING signaling pathways to the attenuatio

66 mutated neurons revealed normal responses to TLR3 and IFN-alpha/beta stimulation but abnormal respons

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

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

69 ensing pathogen recognition receptors (PRRs) TLR3 and RIG-I specifically respond to poly(I:C) and SeV

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

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

72 to assess the relative contributions of the TLR3 and STING pathways to the attenuation of HSV-1 repl

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

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

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

76 080 and HeLa-M cell lines, in which both the TLR3 and the STING pathways are operational, were used.

77 < 0.01) greater in TR APOE4/4 microglia with TLR3 and TLR4 activators.

78 2 and TRIM38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identifie

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

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

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

82 aired production of cytokines in response to TLR3 and TLR4 stimulation of caspase-8-deficient macroph

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

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

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

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

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

88 TLR3 and TLR9 expression and downstream MYD88 signalling

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

90 -those seen following prenatal activation of TLR3 and/or TLR4.

91 TLR3(-/-) and TLR3(+/+) mice were exposed to chronic hyp

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

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

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

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

96 ificantly reduced both Toll-like receptor 3 (TLR3) and TLR4 mRNA expression at 6 hpi and 12 hpi.

97 n loci known to govern Toll-like receptor 3 (TLR3)- and interferon regulatory factor 7 (IRF7)-depende

98 This triggers Toll-like receptor 3 (TLR3)- and TIR domain-containing adapter-inducing interf

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

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

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

102 Inborn errors of TLR3- and DBR1-mediated central nervous system cell-intr

103 Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underli

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

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

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

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

108 he special organelle-located MAVS, STING and TLR3 are important for clearing viral infections.

109 Whereas TLR9 and TLR3 are released from UNC93B1, TLR7 does not dissociate

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

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

112 that the increase in the frequency of CD19(+)TLR3(+) B cells along with reduced levels of total IgG i

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

114 s interferon (IFN)-beta renders SNORA31- and TLR3- but not STAT1-mutated neurons resistant to HSV-1.

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

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

117 munomodulation with Flt3L, radiotherapy, and TLR3/CD40 stimulation induces an influx of stem-like Tcf

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

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

120 3 interaction was critical for maturation of TLR3 containing EE into LE because TLR3 could not be det

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

122 d on the findings that reduced expression of TLR3 contributes to endothelial apoptosis and pulmonary

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

124 TLR3 deficiency also modified the plasma lipid profile,

125 lamydia inclusions, which is suggestive that TLR3 deficiency leads to enhanced chlamydial replication

126 Finally, we demonstrate using hOE cells that TLR3 deficiency resulted in an increased amount of chlam

127 ts are in line with previous reports linking TLR3 deficiency with herpes simplex virus encephalitis.

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

129 (IFN-lambda2) was significantly increased in TLR3-deficient hOE cells compared to their wild-type cou

130 on levels were significantly dysregulated in TLR3-deficient hOE cells.

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

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

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

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

135 B6 mice possibly suggests the initiation of TLR3-dependent pathway early during P. yoelii infection.

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

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

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

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

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

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

142 Our findings indicated that TLR3 engagement of hPDL cells induced immunosuppressive

143 PDL cells in terms of immunomodulation after TLR3 engagement.

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

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

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

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

148 Poly(I:C) increased TLR3 expression via IL-10 in rat endothelial cells.

149 TLR3 expression was reduced in PAH patient lung tissue a

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

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

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

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

154 e immune response to Chlamydia Disruption of TLR3 function in these cells significantly diminished th

155 ome editing to disrupt Toll-like receptor 3 (TLR3) function in the human oviduct epithelial (hOE) cel

156 PBECs from STRA and PSW had increased TLR3 gene expression and increased secretion of anti-vir

157 t (c.2324C > T) in the Toll-like receptor 3 (TLR3) gene resulting in formation of a premature stop-co

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

159 The heterozygous TLR3 genotype 1377C/T and -7C/A SNPs were less common in

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

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

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

163 pairs cytokine responses to bacteria via the TLR3/IFN pathway, which may prevent resolution of inflam

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

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

166 Endosomal TLR3 in hPDL cells was observed by immunocytochemistry.

167 rease in splenic NK and NKT cells expressing TLR3 in infected B6 mice, suggesting a role for TLR sens

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

169 Our work identifies a novel role for TLR3 in PAH based on the findings that reduced expressio

170 e provide evidence for an unexpected role of TLR3 in promoting the establishment of Plasmodium yoelii

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

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

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

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

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

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

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

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

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

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

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

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

183 TLR3 is highly expressed in the pancreas, suggesting tha

184 3 and the molecule UNC93B1, indicating that TLR3 is required for recognizing poly A:U.

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

186 TLR3 knockdown promoted double-stranded RNA signaling vi

187 a in wild type C57BL/6jRj (B6) compared with TLR3 knockout mice.

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

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

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

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

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

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

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

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

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

197 Cs responded efficiently to stimulation with TLR3 ligands, whereas the responses from the fibroblasts

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

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

200 ssue healing and regeneration, activation of TLR3 may help to attenuate tissue destruction by limitin

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

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

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

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

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

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

207 anistically, miR-19a/b and miR-20a decreased TLR3-mediated NF-kappaB activation by targeting SHCBP1 a

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

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

210 TLR3(-/-) and TLR3(+/+) mice were exposed to chronic hypoxia and SU541

211 tient lung tissue and endothelial cells, and TLR3(-/-) mice exhibited more severe pulmonary hypertens

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

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

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

215 LA-G expression, whereas cycloheximide and a TLR3-neutralizing antibody had no effect.

216 The breed-dependent response involved TLR3, NOS2, LITAF, and IFIH1 in the Fayoumi versus IL8,

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

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

219 Tumour necrosis factor (TNF), like TLR3 or TLR4 agonists, also induced caspase-8-dependent

220 N4BP1 did not suppress TLR3 or TLR4 responses in wild-type macrophages, owing t

221 ies have focused primarily on activating the TLR3 or TLR4 subtypes, to mimic immune responses to vira

222 2), TLR7 or TLR9, but not upon engagement of TLR3 or TLR4.

223 rent from those induced by the viral sensors TLR3 or TLR7-9.

224 In addition to TLR9 agonists, TLR2, TLR3, or TLR4 agonists, as well as TNF-alpha, IL-6, or I

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

226 ns are susceptible to HSV-1, like those from TLR3- or STAT1-deficient patients.

227 s mediated by RIPK1 kinase activity, whereas TLR3- or TLR4-mediated death was dependent on TRIF and R

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

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

230 new mechanism in which a parasite-activated TLR3 pathway promotes blood stage infection along with q

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

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

233 , although they were fully functional in the TLR3 pathway.

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

235 tive contributions of the cGAS-STING and the TLR3 pathways in the attenuation of viral infection may

236 eron genes (STING) and Toll-like receptor 3 (TLR3) pathways.

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

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

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

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

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

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

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

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

245 it is poorly understood how TRAF6 regulates TLR3 responses.

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

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

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

249 Gene knockdown of TLR3, RIGI, or IRF1 decreased monocyte adhesion in endot

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

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

252 This alteration could potentially undermine TLR3 signaling in a dominant-negative fashion.

253 Our results indicate a role for TLR3 signaling in limiting the genital tract fibrosis, s

254 order to investigate the possible role(s) of TLR3 signaling in the immune response to Chlamydia Disru

255 -1 revealed that both the cGAS-STING and the TLR3 signaling pathways are required for the attenuation

256 Therefore, we investigated TLR3 signaling responses in APCs and fibroblasts from th

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

258 (ALI) model was used to test whether TLR2 or TLR3 stimulation alters epithelial barrier function usin

259 TLR3 stimulation did not change TEER in the ALI model.

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

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

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

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

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

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

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

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

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

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

270 production triggered by various TLRs (TLR2, TLR3, TLR4, and TLR7), C-type lectin receptors (Dectin-1

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

272 opment, we determined the frequency of TLR2, TLR3, TLR4, and TLR9 single-nucleotide polymorphisms (SN

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 b1, a chaperone necessary for trafficking of TLR3, TLR7, and TLR9 to endosomes.

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 he anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis i

281 TLR3 (Toll-like receptor 3) is a receptor for double-str

282 e polarized sorting of Toll-like receptor 3 (TLR3) towards the basolateral side of IECs.

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

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

285 udy, we confirmed an increased expression of Tlr3, Trif, Tbk1, and Irf7/Irf3 in the liver 42 h postin

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

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

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

289 the host, with deleterious mutations in the TLR3/type I IFN axis underlying some cases of childhood

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

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

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

293 It is well known that TLR3 uses the adaptor protein Toll/interleukin-1 recepto

294 Knockdown of TLR3 using siRNA decreased the poly I:C-induced expressi

295 We report a novel TLR3 variant associated with recurrent zoster ophthalmic

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

297 Interestingly, in the absence of TLR3, we showed the involvement of high IFN-gamma and lo

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