ライフサイエンスコーパス: TLR

1 TLR activation using LPS as a ligand represented a patho

2 TLR agonists are effective at treating superficial cance

3 TLR and IL-1R responses are weak but not abolished in mi

4 TLR ligands, but not proteases, induced TNF during aller

5 TLR-stimulated macrophages from CD11B SNP carriers showe

6 TLRs also have roles in development in many species.

7 TLRs are also expressed on B cells, and TLR signaling in

8 d by real-time PCR and Toll like receptor 4 (TLR-4) protein expression by Western blotting.

9 bility was mediated by toll-like receptor 4 (TLR-4)/MyD88 signal-transduction pathway up-regulation o

10 ultaneously, activated Toll-Like Receptor-4 (TLR-4) on APCs to release chemokine's/cytokines as an im

11 In this work, human Toll-Like Receptor-4 (TLR-4), a protein responsible for detecting lipopolysacc

12 G motifs (CpGs) engage Toll-Like Receptor 9 (TLR-9) in endosomes and are well described stimulators o

13 d CNPYb, we postulated that CNPYb would be a TLR-specific cochaperone of gp93.

14 liferation of early adenomatous lesions in a TLR-dependent manner.

15 ontrast, induction of IDO1 using CTLA-4 or a TLR-3 ligand dampened proinflammatory responses.

16 TRAF6, a TLR effector with ubiquitin (Ub) ligase activity, is ove

17 Chemoimmunomodulation with a TLR-7 agonist and albumin bound paclitaxel is effective

18 PBMCs from MS patients stimulated with a TLR-9 agonist showed reduced expression of general contr

19 to radiation enhances survival by activating TLR signaling, whereas radiomitigating TLR-activating th

20 CPT17e) capable of simultaneously activating TLRs 3, 8, and 9.

21 s known about how these cathelicidins affect TLR activation in the context of complete and viable bac

22 levels and suppresses IL-1beta release after TLR agonism.

23 Although TLR TIR is central to a number of TLR signaling cascades

24 TLRs are also expressed on B cells, and TLR signaling in B cells contributes to antibody-mediate

25 R adaptors by PumA impedes both cytokine and TLR receptor signalling, highlighting a novel strategy f

26 RNA levels of pro-inflammatory cytokines and TLR-4 while increased that of IL-10 after LPS stimulatio

27 tudy, we examined the role of type I IFN and TLR trafficking and signaling in xenobiotic systemic mer

28 permeability was inhibited in MLCK(-/-) and TLR-4(-/-) mice.

29 neously targeting key factors in the RLR and TLR pathways.

30 nses by targeting key factors in the RLR and TLR pathways.

31 Of importance, the risk of TLF and TLR for patients with BVS was higher between 1 and 2 yea

32 ILC2s expressed TLR1, TLR4, and TLR6, and TLR stimulation induced IL-5 and IL-13 production.

33 Combined targeting of UBAP1 and TLR adaptors by PumA impedes both cytokine and TLR recep

34 he simultaneous ligation of several CLRs and TLRs, the signals emanating from different pattern recog

35 y the functional correlation between Mer and TLRs in the development of GC responses and autoimmunity

36 antly associated with inhibition of NODs and TLRs, whereas increased abundance of Streptococcus corre

37 The distribution of SP and TLRs in the nasal mucosa and local airway neurons was as

38 1alpha, IL-6 and IL-8 mRNA levels as well as TLR-4 protein expression were significantly higher while

39 e is also affected by the cross-talk between TLRs and estrogen signalling.

40 Upon ligand binding, TLRs and IL-1Rs recruit adaptor proteins, such as myeloi

41 On pathogen binding, TLRs initiate specialized cytokine signaling catered to

42 ine protein kinase TAK1 in monocytes blocked TLR-induced cytokine production and IRF5 translocation t

43 ized pathogens by immune cells triggers both TLR and Fc receptor signaling.

44 plays a redundant role downstream from both TLRs and IL-1Rs in leukocytes.

45 The protection imparted by TLR ligands persisted for up to 15 d yet was independent

46 c cell (DC) maturation commonly initiated by TLR signaling.

47 e in intestinal permeability was mediated by TLR-4/MyD88 signal-transduction pathway up-regulation of

48 signaling in coordinating RNA processing by TLR pathways during an immune response and in premaligna

49 munosuppressive polarization was reverted by TLR engagement, and M1-oriented macrophages fully activa

50 sight into the regulation of angiogenesis by TLRs and confirm a central role of Fli1 in regulating va

51 endosomes, type III IFNs could be induced by TLRs that reside at the plasma membrane and that detect

52 y stimuli by marking them for recognition by TLRs.

53 ugh these two cell types respond to a common TLR stimulus.

54 m multiple hydrogen bonds, thus crosslinking TLRs into functional complexes.

55 that which drives canonical MYD88-dependent TLR signaling in contemporary mammalian lineages.

56 on induced by injection of several different TLR agonists, including those for TLR2, TLR7, and TLR9.

57 d cross-talk between FcalphaRI and different TLRs, leading to cell type-specific amplification of pro

58 ormation is known about whether differential TLR signaling can selectively inhibit Th17 and/or Th1 ce

59 lular internalization, making them effective TLR-9 immunomodulatory agents.

60 ed the capacity of nanoparticle-encapsulated TLR ligands (NP) to induce potent and durable antibody r

61 y explain the previously described endosomal TLR-mediated resistance to L. major infection.

62 ed for appropriate localization of endosomal TLRs, but the mechanisms are unknown.

63 Serum endotoxin, TLR-4 levels, and inflammatory markers were highest in W

64 t thrombocytes (nucleated platelets) express TLRs and respond to both bacterial and viral products.

65 l responses from multiple, unique fabricated TLR sensor surfaces against the same analyte.

66 Following TLR stimulation, CD1(+) cDC produced IL-8 and IL-10 whil

67 that CXCL4 exposure can sensitize moDCs for TLR-ligand responsiveness, as illustrated by a dramatic

68 MyD88 is the main adaptor molecule for TLR and IL-1R family members.

69 rate that its presence targets molecules for TLR detection, while its absence enables escape of innat

70 pid tails of DNA amphiphiles (CpG motifs for TLR-9 stimulation) into the hydrophobic regions of Pluro

71 hogenesis of PHH, demonstrate a new role for TLRs in regulation of the internal brain milieu, and ide

72 Here we show that exosomes from TLR stimulated cells can largely recapitulate TLR activa

73 at human IRAK-1 is essential downstream from TLRs but not IL-1Rs in fibroblasts, whereas it plays a r

74 Whereas type I IFNs were only expressed from TLRs present on endosomes, type III IFNs could be induce

75 ndings lead to a better understanding of how TLR-ligand based adjuvants can alter and modulate immune

76 domain of Nv-TLR can interact with the human TLR adapter proteins MAL and MYD88.

77 These sensors represent the first hybridized TLR sensors.

78 e extensive clinical use of imidazoquinoline TLR agonists for other indications, these studies identi

79 mulation development of the imidazoquinoline TLR-7/8 agonist 3M-052, in combination with H5N1 hemaggl

80 model of systemic autoimmunity and implicate TLR-mediated NF-kappaB proinflammatory signaling from th

81 b addition in gp93-expressing cells improved TLR expression.

82 TC10 can compensate for the lack of Cdc42 in TLR-induced cell activation and proliferation, so the tw

83 cells lacking the BCR are also defective in TLR-induced B cell activation.

84 Sustained augmentation of glycolysis in TLR-primed cells was dependent, in part, on hypoxia-indu

85 and regulatory regions of genes involved in TLR signaling in resting UCB monocytes.

86 of the K(d)M282-90 CD8(+) T cell response in TLR agonist-treated neonates could be blocked with Abs a

87 ntly expressed in human microglia, including TLR, Fcgamma and SIGLEC receptors, as well as TAL1 and I

88 ion of multiple immune parameters, including TLRs, B cells, CD4(+) cells, IFN-gamma, and NO, on the l

89 ple pattern-recognition receptors, including TLRs and NLRs.

90 proteins, and these iPSC lines do not induce TLR-mediated inflammatory cytokine responses or inflamma

91 horylated in response to the agonist-induced TLR signaling.

92 es were target vessel myocardial infarction, TLR, and cardiac death.

93 at NLRP11, a primate specific gene, inhibits TLR signalling by targeting TRAF6 for degradation.

94 Interestingly, TLR inhibitors did not impact ROS and NET release.

95 e were investigated, understanding the known TLR-PAMP interactions, through the exploitation of this

96 as crucial intermediary processes that link TLR stimulation to DC maturation and the subsequent deve

97 o-fluorobenzene (DNFB) depends on microbiota/TLRs and evaluated the role of TLR4 on the tolerogenic f

98 entation on the electrode surface, mimicking TLR-4's role in a cellular context, was essential in pro

99 secretion after stimulation with mitogenic, TLR, and T-cell stimuli by cytometric bead array.

100 oxygen species (ROS) production and modulate TLR responses, but whether these enzymes function in TLR

101 dins, have previously been shown to modulate TLR activation by synthetic or purified TLR ligands and

102 were highly induced (>3 fold) by one or more TLR ligands, among which 19 of them belong to TRIM C-IV

103 deficiencies of IRAK-4 or MyD88 abolish most TLR (except for TLR3 and some TLR4) and IL-1R signaling

104 Although stimulation with most TLR agonists resulted in strong cytokine mRNA responses,

105 gnaling pathways that are downstream of most TLRs, we hypothesized that miR-718 helps regulate the in

106 ants and anticancer therapies based on multi-TLR activation.

107 b8a and PI3Kgamma are positioned in multiple TLR pathways, and this signaling axis may serve as a pha

108 small molecules that could activate multiple TLRs, we performed a cell-based high-throughput screenin

109 amycin (mTOR) pathway downstream of multiple TLRs.

110 erythematosus and a Syk inhibitor blocked NA-TLR localization with FcgammaRIIIa.

111 gammaRIIIa-pSyk cosignaling in modulating NA-TLR responses in human CD4(+) T cells by affecting the a

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

113 Subcellular location of NA-TLRs is a key determinant in discriminating self versus

114 C3H/HeOuJ mice with normal TLR-4 and C3H/HeJ (Lps-d) with dysfunctional TLR4 (TLR4

115 results highlight the potential for such NP TLR L adjuvants in promoting robust and durable antibody

116 ecific multicellular structure, expresses Nv-TLR and many innate immune pathway homologs and can engu

117 llular Toll/IL-1 receptor (TIR) domain of Nv-TLR can interact with the human TLR adapter proteins MAL

118 al flagellin can activate a reconstituted Nv-TLR-to-NF-kappaB pathway in human cells.

119 ticus Morpholino knockdown indicates that Nv-TLR also has an essential role during early embryonic de

120 immunostaining of anemones, we show that Nv-TLR is expressed in a subset of cnidocytes and that many

121 bset of cnidocytes and that many of these Nv-TLR-expressing cells also express Nv-NF-kappaB.

122 haracterized the single N. vectensis TLR (Nv-TLR) and demonstrated that it can activate canonical NF-

123 s required for restricting the activation of TLR and BCR signaling pathways and the AKT/FOXO1 pathway

124 ranscription factor NFAT5 as an activator of TLR-induced responses, and in this study we explore its

125 terval, 1.31-2.28; P=0.0001; I(2)=0%) and of TLR (odds ratio, 1.27; 95% confidence interval, 1.00-1.6

126 We examine the radiomitigation capability of TLR agonists and identify one that is superior for its e

127 88(-/-)Cardif(-/-) mice, which are devoid of TLR (with the exception of TLR3) and RIG-I-like helicase

128 shed light on the evolution and diversity of TLR pathway signaling elements.

129 cating that autophagy operates downstream of TLR signaling and is relevant for disease development in

130 This study aimed to determine the effects of TLR-activated B10 cells on periodontal bone loss in expe

131 es and how differences may alter efficacy of TLR-based vaccine adjuvants.

132 Examination of TLR signaling pathways implicated the canonical NF-kappa

133 The expression of TLR signaling pathways was also linked to CpG-ODN respon

134 n-based redox probe, due to the formation of TLR-4 protein dimers.

135 The unique impact of TLR agonists on neonatal T cell responses is important t

136 us studies have documented the importance of TLR-TLR cross talk, but few studies have specifically ad

137 HNECs within 30 minutes through induction of TLR movement within HNECs.

138 mply a convergent mechanism of inhibition of TLR signaling by T. gondii and IL-10 and suggest potenti

139 itated immunity in vertebrates, knowledge of TLR pathway evolution in other deuterostomes is limited.

140 plus ionomycin, IL-25/IL-33, or a mixture of TLR ligands.

141 e show that these iPSC lines express mRNA of TLR molecules and the Ag-presentation pathway intermedia

142 Although TLR TIR is central to a number of TLR signaling cascades, its role in sensory neurons is p

143 eful cnidarian model to study the origins of TLR signaling because its genome encodes a single TLR an

144 We assessed a panel of TLR and STING agonists (a) for their ability to reprogra

145 The early phase of TLR signaling and the TLR-dependent secretion of IL-10 (

146 Despite the presence of TLR ligands within the microenvironment, tumors progress

147 is a cross-functional negative regulator of TLR and cytokine receptor signaling via degradation of t

148 F-kappaB pathway and a negative regulator of TLR signaling, in ligated TLR9(-/-) mouse gingival tissu

149 The role of TLR signaling in bacterium-induced ROS and NET release n

150 ly regulates transcription at late stages of TLR-induced proinflammatory gene expression and implicat

151 stimulation with SP induced upregulation of TLR expression in HNECs within 30 minutes through induct

152 Upregulation of TLR expression was not evident when cells were treated w

153 rough TLR2, as determined using a variety of TLR-transfected human embryonic 293 cell lines, while th

154 lation includes regulating the activation of TLRs, which are key players in the recognition of invadi

155 (CNPY3) for proper folding and expression of TLRs, but not integrins.

156 shows for the first time the involvement of TLRs expressed on macrophages in the recognition of and

157 oluble TLR2 (sTLR2), a negative modulator of TLRs that we detected in PDE, inhibited PDE-induced, TLR

158 increased and sustained after stimulation of TLRs.

159 ould exhibit a similar suppressive effect on TLR-stimulation and inflammatory cytokine expression fro

160 The immunoregulatory role of Lyst on TLR signaling pathways was confirmed in human cells by C

161 The effects of SP on TLR expression on HNECs were determined by using flow cy

162 Despite thousands of publications on TLRs, the function of TLR10 remains unknown.

163 mphocytes through IL-25/IL-33 stimulation or TLR triggering.

164 MyD88 (myeloid differentiation factor 88) or TLRs (Toll-like receptors), we demonstrate that TLR2 and

165 l optimization and counterscreening of other TLRs produced the first small molecule 17e (CU-CPT17e) c

166 1D due, in part, to impaired proinflammatory TLR signaling in NOD.Ncf1(m1J) macrophages.

167 Additionally, protective TLR ligands induce sustained augmentation of phagocyte m

168 bone marrow-derived macrophages, protective TLR ligands induced a persistent metabolic phenotype cha

169 Mice primed with protective TLR ligands, including CpG-ODN, showed reduced plasma cy

170 late TLR activation by synthetic or purified TLR ligands and may play an important role in the regula

171 ating TLR signaling, whereas radiomitigating TLR-activating therapeutics given after exposure are les

172 LR stimulated cells can largely recapitulate TLR activation in distal cells in vitro.

173 sent study, the roles of toll-like receptor (TLR) 2, TLR4 and MyD88, in exacerbation of allergen-indu

174 Therefore, the role of Toll-like receptor (TLR) 2, TLR4, myeloid differentiation response gene 88,

175 tion of calprotectin and Toll-like receptor (TLR) 4 in inflamed skin.

176 57BL/6 J wild-type mice, Toll-like receptor (TLR) 4 knockout (Tlr4(-/-)) mice, and recombination-acti

177 pendent of both upstream Toll-like receptor (TLR) 4 signaling and downstream type I interferon (IFN)

178 LPS binds Toll-like receptor (TLR) 4, which leads to the release of proinflammatory cy

179 olecule imidazoquinoline Toll-like receptor (TLR) 8 agonists robustly activate newborn DCs but can re

180 Toll-like receptor (TLR) activation contributes to premalignant hematologic

181 Toll-like receptor (TLR) activation stimulates antiviral immunity and has be

182 ble to interact with the Toll-like receptor (TLR) adaptors TIRAP and MyD88, as well as the ubiquitin-

183 n of the inflammasome by Toll-like receptor (TLR) agonism with bacterial lipopolysaccharide (LPS) and

184 Toll-like receptor (TLR) agonist adjuvant formulations have a demonstrated a

185 se (iNOS) mRNA following Toll-like receptor (TLR) agonist treatment.

186 to oxidative stress and toll-like receptor (TLR) agonist.

187 ith several Th1-inducing Toll-like receptor (TLR) agonists in vivo In mice, the TLR9 agonist cytosine

188 rs through their role in Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) mediated signali

189 Most members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transdu

190 , the common adaptor for toll-like receptor (TLR) and Interleukin-1 receptor signaling, are critical

191 ive regulator of ILR and Toll-like receptor (TLR) downstream signalling pathways and inflammation.

192 ition by flow cytometry, Toll-like receptor (TLR) expression by quantitative PCR, and cytokine secret

193 cted in changes in local Toll-like receptor (TLR) expression.

194 TOLL-like receptor (TLR) ligands activate both innate and adaptive immune ce

195 e-agonists, specifically Toll-like receptor (TLR) ligands, using biodegradable, polymer microparticle

196 s activated by different toll-like receptor (TLR) ligands.

197 Cross-regulation of Toll-like receptor (TLR) responses by cytokines is essential for effective h

198 evidence indicates that Toll-like receptor (TLR) signaling adapter protein interactions with Toll/In

199 The role of Toll-like receptor (TLR) signaling in processing of SLE ICs and downstream i

200 termined the function of Toll-like receptor (TLR) signaling on the progression of Kras-induced early

201 as a central function in Toll-like receptor (TLR) signalling, yet the molecular mechanisms controllin

202 ed both before and after Toll-like receptor (TLR) stimulation.

203 ling pathways, including Toll-like receptor (TLR), mitogen-activated protein kinase, Jak-STAT, and th

204 ritical roles in virus-, Toll-like receptor (TLR)-, and IFN-induced signaling pathways.

205 Dysregulated Toll-like receptor (TLR)-4 activation is involved in acute systemic sepsis,

206 opolysaccharide (LPS), a Toll-like receptor (TLR)-4 agonist.

207 were stimulated with the toll-like receptor (TLR)-4 ligand, lipopolysaccharide (LPS), in the presence

208 y cancers with a topical toll-like receptor (TLR)-7 agonist, imiquimod.

209 ndent antigens through a Toll-like receptor (TLR)-amplified pathway involving transmembrane activator

210 Toll-like receptor (TLR)-mediated sensing of the microbiota contributes to g

211 ociated genes, including toll-like receptor (TLR)2, the receptor for advanced glycation end products

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

213 ibitors of intracellular toll-like receptor (TLR)9.

214 Toll-like receptors (TLR) are conserved immune sensors mediating antimicrobia

215 hieved using hybridized toll-like receptors (TLR) combining TLR1 and TLR2 onto a single sensor surfac

216 ry mediators binding to Toll-Like receptors (TLR) induce an influx of superoxide anion in the ensuing

217 r engagement of CD40 or Toll-like receptors (TLR), despite paradoxically enhanced plasma cell differe

218 r the two components is Toll-like receptors (TLR), which are key regulators of the innate immune syst

219 the fundamental role of Toll-like receptors (TLRs) and complement in inflammation, we assessed the po

220 lient proteins, such as Toll-like receptors (TLRs) and integrins, in a gp96-deficient murine cell lin

221 ent work has identified Toll-like receptors (TLRs) and type I interferon (IFN) signaling in both isch

222 onding to pathogens and Toll-like receptors (TLRs) are a critical component of this response.

223 Toll-like receptors (TLRs) are innate immune receptors for sensing microbial

224 Toll-like receptors (TLRs) are major players of the innate immune system.

225 insects to vertebrates, Toll-like receptors (TLRs) are primary pathogen detectors that activate downs

226 mediate the function of Toll-like receptors (TLRs) except TLR3, contained VH4-34-expressing clones an

227 ention of intracellular Toll-like receptors (TLRs) in the endoplasmic reticulum prevents their activa

228 activation of multiple Toll-like receptors (TLRs) may offer superior therapeutic profiles than that

229 Toll-like receptors (TLRs) play an important role in B cell-mediated immune r

230 Toll-like receptors (TLRs) play an important role in immune responses to path

231 ted upon acutely by the Toll-like receptors (TLRs) to halt proliferation and activate an immune respo

232 at can be recognized by Toll-like receptors (TLRs), engulfment of ACs does not initiate inflammation

233 in signaling by several Toll-like receptors (TLRs), key pattern recognition receptors (PRRs).

234 When activated through toll-like receptors (TLRs), macrophages generate IL-33, an IL-1 family member

235 Pathogen-activated Toll-like receptors (TLRs), such as TLR2 and TLR4, dimerize and move laterall

236 ated molecules, such as Toll-like receptors (TLRs), the complement system, cytokines, chemokines, inf

237 e-associated mucins and Toll-like receptors (TLRs).

238 One such family is the Toll-like receptors (TLRs).

239 ators and inhibitors of Toll-like receptors (TLRs).

240 CD11b activation reduced TLR-dependent proinflammatory signaling in leukocytes an

241 ceptors, low expression of TLR9, and reduced TLR responsiveness to nucleic acids.

242 emia-driven target lesion revascularization [TLR]).

243 t of type I IFN and the nucleic acid sensing TLRs, blocking these pathways rescues the autoimmunity.

244 Type I IFN and nucleic acid-sensing TLRs are both strongly implicated in the pathogenesis of

245 on of adaptive immune responses with several TLR agonists acting as known B cell mitogens.

246 e in germ-free and mice deficient in several TLRs.

247 ion in response to signaling through several TLRs.

248 ignaling because its genome encodes a single TLR and homologs of many downstream signaling components

249 ior therapeutic profiles than that of single TLR activation.

250 At these sites, TLRs interact with the TIR domain-containing adaptor pro

251 nalyses corroborate several lineage-specific TLR gene expansions in urchins and cephalochordates.

252 us linking phagosomal maturation to specific TLR signaling pathways.

253 nd lipid mediators in response to subsequent TLR stimulation.

254 the lipoylated E2 subunit of PDH to suppress TLR-mediated activation of host macrophages by bacterial

255 iated kinase (IRAK)-M is induced to suppress TLR-mediated responses and is a hallmark of endotoxin to

256 ic miRNAs are estrogen responsive and target TLR (toll-like receptor) signaling pathways.

257 These data suggest that targeting TLR TIR domains may provide novel pharmacological target

258 tro, ex vivo, and in vivo analyses show that TLR-induced DC maturation, as assessed by surface phenot

259 ERT2-Cre/dTomato fate-mapping mice show that TLR-initiated DC autocrine C3ar1/C5ar1 signaling causes

260 The early phase of TLR signaling and the TLR-dependent secretion of IL-10 (controlled by IRAKs 1

261 r function for exosomes in communicating the TLR activation state of the cell of origin.

262 a (TRIF), factors critically involved in the TLR signaling pathway, was studied in experimental autoi

263 ther, the study provided an insight into the TLR ligands-induced expressions of TRIM family in macrop

264 and pathways, including LPS, members of the TLR and PPAR families, NF-kappaB, and TNF-related weak i

265 sions of genes encoded for components of the TLR, nucleotide binding oligomerization domain-like rece

266 1 through a pathway that is dependent on the TLR signaling adaptor MyD88 and its downstream kinase IL

267 ceptor signaling pathways in response to the TLR ligands listed above.

268 IRAP, suggesting that it is recruited to the TLR signalosome by multitypic TIR-TIR interactions.

269 This receptor interacts with mTOR via the TLR adapter MyD88.

270 us as well as following stimulation with the TLR ligands Poly(I:C) and CpG.

271 Innate regulation through TLR signaling has been shown to be important for promoti

272 Differences in ion dependences between TL/TLR variants indicated the occurrence of sequence-depend

273 Our results revealed a multistep TL/TLR folding pathway in which preorganization of the ubiq

274 motif, the tetraloop/tetraloop-receptor (TL/TLR).

275 less, varying the junction connecting the TL/TLR produced a common kinetic and ionic effect for all v

276 nic conditions, and the occurrence of the TL/TLR sequence variants in Nature correlates with their th

277 Exposure of bdMphi to TLR agonists and/or bdIFNgamma resulted in upregulated c

278 We report that galectin-3 can bind to TLR-4, and that administration of a neutralizing antibod

279 of antimicrobial immunity after exposure to TLR ligands.

280 Already prior to TLR- or Ag-specific stimulation, CXCL4-moDCs displayed a

281 n alarmin, binding, among other proteins, to TLR-4 and promoting inflammation and neuronal loss.

282 enerate a reduced IL-6/TNF-alpha response to TLR 1/2 and 4 ligands compared to those collected from l

283 activating neonatal LTi cells in response to TLR stimulus.

284 control type I IFN expression in response to TLRs.

285 adaptor protein-3 complex, which transports TLRs from the early endosome to the late endolysosomal c

286 The combination of the two TLR agonists allows for significant dose reductions of e

287 te significant advances toward understanding TLR-facilitated immunity in vertebrates, knowledge of TL

288 Unlike TLRs located on the plasma membrane that dimerize on the

289 dritic cells (DCs) and plasmacytoid DCs upon TLR-mediated activation and detectable by Nkrp1g, which

290 ice sensitized to an innocuous protein using TLR ligands or house dust extracts as adjuvants develope

291 5 also suppressed the stimulation of various TLRs in response to whole bacteria extracts, suggesting

292 e have characterized the single N. vectensis TLR (Nv-TLR) and demonstrated that it can activate canon

293 n the present study, we investigated whether TLR-4 deficiency reduces Ang-II-induced renal injury and

294 is study we investigated the degree to which TLR TIR decoy peptide modified to include a TAT sequence

295 With TLR ligation, the deubiquitinase enzyme, STAM-binding pr

296 FN-alpha, possibly through interference with TLR signaling and recruitment of IRF7 and p85 into lysos

297 find that using APC pretreated ex vivo with TLR agonists, polyinosinic-polycytidylic acid and CpG, t

298 ced genes in peripheral blood cells and with TLRs promoting type I IFNs and autoreactive B cells.

299 signaling via NF-kappaB and cooperation with TLRs, thereby hampering IgG production to T-cell-indepen

300 Following ligand interaction with TLRs, TIR serves to both initiate intracellular signalin