ライフサイエンスコーパス: TLR8

1 gnition receptor (PRR) Toll-like receptor 8 (TLR8).

2 s, confirming its high selectivity for human TLR8.

3 ic mice expressing different levels of human TLR8.

4 ecently described crystal structure of human TLR8.

5 through Toll like Receptors (TLR)3, TLR7 and TLR8.

6 was maximally antagonistic at both TLR7 and TLR8.

7 hages expressing both intracellular TLR7 and TLR8.

8 intracellular receptor in human subjects is TLR8.

9 he ligands for Toll-like receptor (TLR)7 and TLR8.

10 r natural guanosine activated human TLR7 and TLR8.

11 lines can selectively activate human TLR7 or TLR8.

12 se data, ASMC expressed TLR3 but not TLR7 or TLR8.

13 s (DCs) through interaction with TLR7 and/or TLR8.

14 as hampered our understanding of the role of TLR8.

15 requisites governing activity at TLR7 and/or TLR8.

16 ized for their activity and selectivity over TLR8.

17 TLR8 1A/G reduced disease progression.

18 ted by 3M-002 (TLR8 agonist) and resiquimod (TLR8/7 agonist).

19 that activate TLR8 (R-848; (TLR7/8) CL075; (TLR8/7)), with respect to activation of human newborn an

20 2L:Pam3CSK4, TLR5L:flagellin, TLR4L:LPS, and TLR8/7L:CL075 also blocked Treg suppression of CD4(+) or

21 On the cellular level, TLR8(-/-) and TLR8/9(-/-) dendritic cells were hyperesponsive to TLR7

22 Moreover, B cells from TLR9(-/-) and TLR8/9(-/-) mice were hyperesponsive to R848, but TLR8(-

23 ere, we reveal that double TLR8/9-deficient (TLR8/9(-/-)) mice on the C57BL/6 background showed incre

24 Here, we reveal that double TLR8/9-deficient (TLR8/9(-/-)) mice on the C57BL/6 backg

25 blood, consistent with an active circulating TLR8/9-stimulating factor.

26 blood mononuclear cells, but only TLR7- and TLR8-activating compounds activated plasmacytoid dendrit

27 Additionally, TLR7- and TLR8-activating compounds, but not the compounds that ac

28 However, TLR8 activation by R-848 and TLR2 activation by [S-[2,3-

29 e protease granzyme B upon both FcgammaR and TLR8 activation.

30 lper 1-polarizing cytokines, suggesting that TLR8-active compounds may be promising candidate adjuvan

31 In an effort to identify novel dual TLR7/TLR8-active compounds, we undertook structure-activity r

32 es permitted the classification of inactive, TLR8-active, and TLR7/8 dual-active compounds, confirmin

33 ion in mononuclear phagocytes by suppressing TLR8 activity and this particular function of FANCC is i

34 ently described scaffolds that have residual TLR8 activity, which may be detrimental to the tolerabil

35 s ratio [aGMR], 1.15; 95% CI, 1.02-1.30) and TLR8 (aGMR, 1.15; 95% CI, 1.04-1.26).

36 However, a combination of polyT ODN plus the TLR8 agonist activated NF-kappaB, whereas polyT ODN plus

37 Immunogenicity of the TLR8 agonist adjuvanted antigen 85B (Ag85B)/peptide 25-l

38 ves, TLR7-deficient mice are unresponsive to TLR8 agonist IRMs.

39 Remarkably, TLR8 agonist polymersomes induced not only newborn DC ma

40 VTX-294 is a novel ultra-potent TLR8 agonist that activates newborn and adult leukocytes

41 tuximab-coated tumor targets was enhanced by TLR8 agonist treatment, and this enhancement of ADCC req

42 r, we found that LC are activated by 3M-002 (TLR8 agonist) and resiquimod (TLR8/7 agonist).

43 cterize polymer nanocarriers encapsulating a TLR8 agonist, allowing direct intracellular release afte

44 odo-6-methylpyrimidine-2,4-diamine as a pure TLR8 agonist, and a detailed structure-activity relation

45 o[d]imidazol-2-amine, was found to be a pure TLR8 agonist, evoking strong proinflammatory cytokine an

46 We demonstrate that a selective TLR8 agonist, in combination with FLT3L, primes high-qua

47 djuvant, with or without a TLR7/8 agonist, a TLR8 agonist, or the TLR9 ligand cytosine phosphate guan

48 timulatory activities of a novel benzazepine TLR8 agonist, VTX-294, in comparison to imidazoquinoline

49 subcutaneous injection to neonatal mice, the TLR8 agonist-adjuvanted Ag85B peptide 25 formulation was

50 rrow-derived DCs enabled benchmarking of the TLR8 agonist-encapsulating polymersome formulations agai

51 uptake by murine DCs in vivo, and a range of TLR8 agonist-encapsulating polymersome formulations were

52 TLR8 agonist-encapsulating polymersomes hold substantial

53 The ontogeny of TLR8 agonist-induced cytokine responses was defined in r

54 at the same time with either of the TLR7 or TLR8 agonist.

55 mine was found to be a very potent dual TLR7/TLR8 agonist.

56 esent a novel, alternate chemotype with pure TLR8-agonistic activities and will likely prove useful n

57 We observed a pure TLR8-agonistic activity profile in select furo[2,3-c]qui

58 nopropyl appendages at C5 displayed dominant TLR8-agonistic activity.

59 When stimulated with TLR7 or TLR8 agonists alone, no NF-kappaB response was observed.

60 TLR8 agonists also effectively induced up-regulation of

61 LR8 that does not respond to any known human TLR8 agonists also inhibits both murine and human TLR7.

62 TLR8 agonists are more effective than other TLR agonists

63 We conclude that TLR8 agonists are uniquely efficacious in activating cos

64 mice overexpressed TNF-alpha in response to TLR8 agonists but not other TLR agonists.

65 esion clearance may differ and that TLR7 and TLR8 agonists can reduce the frequency of mucosal HSV-2

66 The strong activity of TLR8 agonists correlates with their induction of p38 MAP

67 Thus, this study demonstrated that TLR7 and TLR8 agonists differ in their target cell selectivity an

68 Interestingly, some of the TLR7 and/or TLR8 agonists differed in their ability to activate glia

69 Conversely, TLR8 agonists directly activated purified myeloid dendri

70 Treatment with TLR8 agonists elicited granzyme B and also enhanced Fcga

71 IMQ TLR8 agonists engage adenosine-refractory TLR8 and infla

72 erebroventricular inoculation of TLR7 and/or TLR8 agonists in newborn mice.

73 Incorporation of TLR3 and TLR8 agonists into the CD40L/IFN-gamma activation protoc

74 Dual TLR7/TLR8 agonists markedly upregulate CD80 expression in mul

75 but little is known about whether different TLR8 agonists may distinctly activate neonatal leukocyte

76 nd have uncovered another mechanism by which TLR8 agonists may enhance FcgammaR-based therapies.

77 The TLR8 agonists polyuridylic acid and polyadenylic acid al

78 dy, we examined the potential of TLR7 and/or TLR8 agonists to induce glial activation and neuroinflam

79 ld be considerably more favorable than other TLR8 agonists under evaluation.

80 acholine in vitro, and responses to TLR7 and TLR8 agonists were assessed.

81 In contrast, TLR8 agonists were more effective than TLR7 agonists at

82 TLR8 agonists, including imidazoquinolines (IMQs), such

83 We now show that TLR8 agonists, including R-848 (TLR7/8), the imidazoquin

84 HEK293 cells transfected with murine TLR7 or TLR8 and a NF-kappaB luciferase reporter, we demonstrate

85 ociations exist between genetic variation in TLR8 and AR.

86 TLR8 and inflammasome function were assayed by using sma

87 MQ TLR8 agonists engage adenosine-refractory TLR8 and inflammasome pathways to induce robust monocyte

88 This occurs through TLR8 and leads to the production of TNF-alpha and IL-6,

89 Human TLR7 and TLR8 and mouse TLR7 recognize viral ssRNA motifs and ind

90 udy, we transfected HEK293 cells with murine TLR8 and NF-kappaB reporter constructs and stimulated th

91 pha production in mutant cells depended upon TLR8 and the canonical downstream signaling intermediate

92 Triggering of Toll-like receptor (TLR) 4 or TLR8 and the proinflammatory cytokines IL-1beta or IL-6

93 and TLR9 control TLR7 function, but whether TLR8 and TLR9 act in parallel or in series in the same o

94 Thus, both TLR8 and TLR9 control TLR7 function, but whether TLR8 an

95 These results reveal that TLR8 and TLR9 have an additive effect on controlling TLR

96 ic ligands for TLR2, TLR3, TLR4, TLR5, TLR7, TLR8 and TLR9 in the presence or absence of telomeric ol

97 enting cells through the RNA and DNA sensors TLR8 and TLR9.

98 that respond to viral infection, TLR3, TLR7, TLR8 and TLR9.

99 On the cellular level, TLR8(-/-) and TLR8/9(-/-) dendritic cells were hyperespo

100 e toll-like receptor system (TLR4, TLR7, and TLR8) and inflammasome complex pathway (NLRP3, NLRC4, an

101 ions of the endovesicular Toll-like receptor TLR8, and the inflammasome protein NAcht leucine-rich re

102 ts displayed dysregulated responses to TLR4, TLR8, and TLR7 stimulation.

103 activate the innate immune system via TLR7, TLR8, and TLR7/8, respectively.

104 Destruction of YxxPhi abolished TLR7, TLR8, and TLR9 activity toward nucleic acids in human B

105 b(+) cells that respond to TLR2, TLR4, TLR7, TLR8, and TLR9 agonists as measured by the secretion of

106 ILshort production are type I IFNs and TLR7, TLR8, and TLR9 agonists.

107 show that in CD4(+) T cells, NA-TLRs, TLR3, TLR8, and TLR9 are upregulated by FcgammaRIIIa-pSyk cosi

108 Among the 11 human TLRs, a subfamily TLR7, TLR8, and TLR9 display similarities in structure and end

109 fter exposure to Toll-like receptor (TLR) 2, TLR8, and TLR9 ligands, further supporting an important

110 Hence, TLR7, TLR8, and TLR9 may prevent the recruitment of developing

111 g at the effect of the agonists of the TLR7, TLR8, and TLR9 on the activation of NF-kappaB of transfe

112 Toll-like receptor (TLR)7, TLR8, and TLR9 sense microbial or endogenous nucleic aci

113 lar PRRs such as endosomal TLRs (TLR3, TLR7, TLR8, and TLR9) and cytoplasmic proteins (absent in mela

114 or several TLRs, including TLR3, TLR4, TLR7, TLR8, and TLR9, have been or are being developed for the

115 atory DNA sequences (IRSs) specific to TLR7, TLR8, and TLR9, we show that the TLR8 inhibitor IRS957 s

116 er localization of intracellular TLR3, TLR7, TLR8, and TLR9.

117 icient cells are unresponsive to TLR3, TLR7, TLR8, and TLR9.

118 sely related and highly homologous are TLR7, TLR8, and TLR9.

119 effects of one TLR on the other among TLR7, TLR8, and TLR9.

120 Demonstrating that TLR7 and TLR8 are expressed on human LC, we hypothesized that imi

121 Rare variants in TLR8 are not associated with AR.

122 Although TLR7 and TLR8 are phylogenetically and structurally related, thei

123 quent downstream signaling by human TLR7 and TLR8 are unknown.

124 Other receptors (in addition to TLR7 and TLR8) are likely to be found, but this is the first iden

125 nd overexpression, we unambiguously identify TLR8 as receptor for bacterial RNA in primary human mono

126 noline congeners 3M-003 (TLR7/8) and 3M-002 (TLR8), as well as single-stranded viral RNAs (TLR8) indu

127 n mutant cells, we confirmed that TLR8 (or a TLR8-associated protein) is ubiquitinylated in mutant FA

128 tiated HL-60 cells express RIG-I, MDA-5, and TLR8 at the mRNA and protein levels, whereas TLR3 and TL

129 9(-/-) mice were hyperesponsive to R848, but TLR8(-/-) B cells were not.

130 Taken together in human macrophages, TLR8 binds and internalizes HIV ssRNA, leading to endoso

131 at RNA signals through human TLR3, TLR7, and TLR8, but incorporation of modified nucleosides m5C, m6A

132 A3hi DCs respond to poly I:C and agonists of TLR8, but not of TLR7, and produce interleukin (IL)-12 w

133 compared with linear RNA and activated human TLR8, but not TLR7, in HEK293 cells without using lipid

134 signaling (SOCS)-1 directly associated with TLR8, but not with TLR7, indicating a novel role for TLR

135 eporter, we demonstrated that stimulation of TLR8-, but not TLR7-, transfected cells with either VV o

136 hich synthetic and natural ligands for human TLR8 can reverse Treg cell function.

137 Our data suggest TLR7 and TLR8 can signal in two different "modes" depending on th

138 rophages expressing TLR4, TLR4/TLR5, or TLR4/TLR8 chimeras but not in macrophages expressing TLR4/TLR

139 Furthermore, knockdown of TLR8 completely attenuated collagen expression in monocy

140 TLR8 controls TLR7 function on dendritic cells, and TLR9

141 Collectively, we report that TLR8 coupling with SOCS-1 inhibits TLR7-mediated antivir

142 In this article, we report that TLR8-deficient (Tlr8(-/-)) mice were resistant to WNV in

143 Moreover, TLR8-dependent detection of bacterial RNA was critical f

144 r BIRB 796 and dasatinib potently suppressed TLR8-dependent expression of the reporter gene.

145 eotides were capable of activating pDCs in a TLR8-dependent manner.

146 Several analogues were found to activate TLR8-dependent NF-kappaB signaling.

147 dendritic cells as well as the production of TLR8-dependent type II interferon (IFN-gamma), TNF-alpha

148 The responses induced by F-HIV were TLR8-dependent with subsequent activation of IFN regulat

149 IFN-gamma and TNF-alpha induction is largely TLR8-dependent.

150 mpounds that activates TLR8 or both TLR7 and TLR8 depending on the nucleotide composition and chemica

151 f Snapin enhanced localization of HIV-1 with TLR8(+) early endosomes, triggered a pro-inflammatory re

152 response to TLR1/2, TLR2/6, TLR3, TLR5, and TLR8 engagement in mDCs and TLR7 and TLR9 in pDCs.

153 Activation of human toll-like receptor-8 (TLR8) evokes a distinct cytokine profile favoring the ge

154 infrequent, and TLR1, TLR3, TLR5, TLR6, and TLR8 expressed in selective patterns.

155 vation, and that siRNA-mediated knockdown of TLR8 expression in pDCs led to a complete ablation of VV

156 th systemic arthritis and the correlation of TLR8 expression with the elevation of IL-1beta levels an

157 ethylation of histone 3 at lysine 4, whereas TLR8 gene knockdown reduced these effects.

158 Either MYD88 or TLR8 gene knockdown with relevant siRNA reduced HIV-1 ss

159 The TLR8 gene was resequenced in 288 AR patients from Malmo

160 TLR8 IMQs induced robust TNF and IL-1beta in whole blood

161 adult monocytes and MoDCs, signaling through TLR8 in an adenosine/cyclic AMP-refractory manner.

162 However, the role of mouse TLR8 in antiviral immunity is poorly understood.

163 Crystal structures of TLR8 in complex with the two most active compounds confi

164 Agonist stimulation of TLR8 in cultured cortical neurons causes inhibition of n

165 a new mechanism of innate immune sensing by TLR8 in DCs, which is exploited by HIV-1 to promote tran

166 converts self-RNA into a trigger of TLR7 and TLR8 in human DCs, and provide new insights into the mec

167 A pathogenic role for TLR8 in human diseases was suggested by its increased ex

168 ind to toll-like receptors (TLR7 in mice and TLR8 in human) expressed by the immune cells.

169 diseases that may benefit from inhibition of TLR8 in humans.

170 Studies on the role of the RNA receptor TLR8 in inflammation have been limited by its different

171 s TLR7 and TLR9 in human dendritic cells and TLR8 in monocytes.

172 RNA receptors RIG-I, MDA-5, TLR3, TLR7, and TLR8 in primary neutrophils and immortalized neutrophil-

173 s a cooperative interaction between TLR2 and TLR8 in pro- and antiinflammatory cytokine responses, wh

174 rus and highlight the importance of TLR7 and TLR8 in that response.

175 These findings reveal novel functions for TLR8 in the mammalian nervous system that are distinct f

176 r study demonstrates a physiological role of TLR8 in the sensing of entire S. aureus in human primary

177 an anti-HCV immune response through TLR7 and TLR8 in various antigen presenting cells.

178 receptor (TLR) family, murine TLR7 and human TLR8, in immune cells, triggering a TLR-mediated prometa

179 aining compound that activated both TLR7 and TLR8 induced IFN-alpha in monkeys.

180 LR8), as well as single-stranded viral RNAs (TLR8) induced robust production of the Th1-polarizing cy

181 ic to TLR7, TLR8, and TLR9, we show that the TLR8 inhibitor IRS957 significantly diminishes productio

182 The results indicate that TLR8 inhibits TLR7 and TLR9, and TLR9 inhibits TLR7 but

183 TLR8 -: IRF5 signaling was necessary for induction of IF

184 emonstrate that the sequence motif sensed by TLR8 is clearly distinct from that recognized by TLR13.

185 We report that TLR8 is dynamically expressed during mouse brain develop

186 poly(A)/T-rich DNA in pDCs, and that murine TLR8 is functional in the context of a viral infection.

187 y demonstrates for the first time that mouse TLR8 is functional.

188 rine TLR8, leading to the belief that murine TLR8 is nonfunctional.

189 y, our data are unique in demonstrating that TLR8 is required for sensing poly(A)/T-rich DNA in pDCs,

190 antiinflammatory cytokine responses, whereas TLR8 is solely responsible for IRF7-mediated induction o

191 erved for polymorphisms in TLR2, TLR4, TLR6, TLR8, ITGAV, ITGB3, ITGAM, and TIRAP.

192 ion into MPhis could be prevented by TLR7 or TLR8 knockdown.

193 ilarly, natural ssRNA cannot activate murine TLR8, leading to the belief that murine TLR8 is nonfunct

194 Adoptive transfer of TLR8 ligand-stimulated Treg cells into tumor-bearing mic

195 TLR8 ligands induced IKKgamma phosphorylation, whereas I

196 TLR8 ligands trigger similar levels of IkappaBalpha phos

197 were required for these cells to respond to TLR8 ligands, whereas TAK1, JNK, and ERK molecules did n

198 R7 and TLR9, but not to TLR2, TLR4, TLR5 and TLR8 ligands.

199 IL-1 were not detected in cells treated with TLR8 ligands.

200 on) were not detected in cells stimulated by TLR8 ligands.

201 Drugs targeting macrophage TLR8-linked signaling pathways may modulate the innate i

202 detected a number of significant SNPs in the TLR8 locus.

203 The TLR8-mediated activation of IRF5 was dependent on TAK1 a

204 On the other hand, TLR8-mediated IkappaBalpha phosphorylation, NF-kappaB, a

205 n induced the expression of pro-IL-1beta via TLR8-mediated mechanisms and activated caspase-1 through

206 We postulate that TLR8-mediated MEKK3-dependent IKKgamma phosphorylation m

207 Our evidence indicates that such TLR8-mediated neuronal responses do not involve the cano

208 The differences between IL-1R- and TLR8-mediated NF-kappaB activation are also reflected at

209 how significant effects on TLR3-, TLR7-, and TLR8-mediated NF-kappaB activation.

210 TLR8-mediated NF-kappaB and IRF7 activation are abolishe

211 ts of IRAK and IRAK4, respectively, restored TLR8-mediated NF-kappaB and IRF7 activation in the IRAK-

212 The above results indicate that although TLR8-mediated NF-kappaB and JNK activation are IRAK-depe

213 The production of IFN-beta was induced by TLR8-mediated sensing of S. aureus RNA, which triggered

214 of IRAK and IRAK4 is probably redundant for TLR8-mediated signaling.

215 We recently found that TLR8 mediates a unique NF-kappaB activation pathway in h

216 eptibility to WNV-mediated neuronal death in Tlr8(-/-) mice were attributed to overexpression of Tlr7

217 this article, we report that TLR8-deficient (Tlr8(-/-)) mice were resistant to WNV infection compared

218 ibe the syntheses and evaluation of TLR7 and TLR8 modulatory activities of dimeric constructs of imid

219 tal human monocyte-derived DCs and humanized TLR8 mouse bone marrow-derived DCs enabled benchmarking

220 urified NK cells despite their expression of TLR8 mRNA and protein.

221 In vivo, TLR8-MyD88-dependent pDC activation played a critical ro

222 t of dendritic cells but required functional TLR8-MyD88-IRAK4 signaling in Treg cells.

223 ion was evaluated in vivo by using humanized TLR8 neonatal mice.

224 ndence of the selectivity for TLR7 vis-a-vis TLR8 on the electronic configurations of the heterocycli

225 ulatory RNA (SIMRA) compounds that activates TLR8 or both TLR7 and TLR8 depending on the nucleotide c

226 ated only in mutant cells, we confirmed that TLR8 (or a TLR8-associated protein) is ubiquitinylated i

227 ls, and renal pathology compared with single TLR8(-/-) or TLR9(-/-) mice.

228 by Toll-like receptor members TLR3, TLR7 and TLR8, or by the RNA helicases RIG-I (also known as DDX58

229 In mice TLR7-deficiency ameliorates SLE, but TLR8- or TLR9-deficiency exacerbates the disease because

230 acuole, whereas recruitment of both TLR2 and TLR8 overlaps with degradation of the spirochete.

231 elated to immune function and transcription (TLR8, P = .0002; DAPP1, P = .0003; LAMP3, P = 9.96E(-05)

232 mmune defenses (e.g., RIG-1, MDA-5, TLR7 and TLR8, PKR, APOBEC3B, 3F, 3G), adaptive immunity, and in

233 ptor (TLR) expression (PMN-I, TLR2/TLR4/TLR5/TLR8; PMN-II, TLR2/TLR4/TLR7/TLR9; PMN-N, TLR2/TLR4/TLR9

234 omparison to imidazoquinolines that activate TLR8 (R-848; (TLR7/8) CL075; (TLR8/7)), with respect to

235 mally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and to IL-1beta.

236 Toll-like receptors TLR7 and TLR8 recognize specific intracellular viral ssRNA sequen

237 therefore searches for rare variants in the TLR8 region and also investigates the reproducibility of

238 t not with TLR7, indicating a novel role for TLR8 regulation of SOCS-1 function, whereas selective sm

239 The modulation of TLR7 and TLR8 responses is independent of CpG motifs or the natur

240 cids in human B cells and monocytes, whereas TLR8 responses toward small molecules remained intact.

241 s and activates dendritic cells via TLR7 and TLR8, resulting in the activation of the NF-kappaB pathw

242 that the consequence of self-recognition via TLR8 results in a constellation of diseases, strikingly

243 ression of Toll-like receptor (TLR) 3, TLR7, TLR8, retinoic acid-inducible gene I (RIG-I), melanoma d

244 The "G-G" haplotype of TLR7 rs3853839 and TLR8 rs3764880 increased risk of SLE in females (age adj

245 TLR7 rs3853839-G (G vs. C: p = 0.0100) and TLR8 rs3764880-G (recessive model: p = 0.0173; additive

246 -selective agonists were more effective than TLR8-selective agonists at inducing IFN-alpha- and IFN-r

247 The absence of TLR8-selective agonists has hampered our understanding o

248 yte-derived dendritic cells here showed that TLR8 sensing of RNA ORN versus imidazoquinoline translat

249 and suppressor function could be blocked by TLR8 signaling and/or by specific ERK1/2 and p38 inhibit

250 ikely prove useful not only in understanding TLR8 signaling but also perhaps as a candidate vaccine a

251 These results suggest that TLR8 signaling could play a critical role in controlling

252 at poly(T) ODNs can inhibit TLR7 and enhance TLR8 signaling events involving NF-kappaB activation in

253 dition, we demonstrated that manipulation of TLR8 signaling in gammadelta Treg cells can block gammad

254 Snapin inhibited TLR8 signaling in the absence of HIV-1 and is a general

255 Of particular interest, the human TLR8 signaling pathway is essential for reversing the su

256 fic gammadelta T cells and identify a unique TLR8 signaling pathway linking to their functional regul

257 This modulation of TLR8 signaling was mediated by complement receptor 3 and

258 ignaling pathway but is activated by TLR7 or TLR8 signaling.

259 3-pentyl-quinoline-2-amine as a novel, human TLR8-specific agonist.

260 lactis G121-treated human DCs was blocked by TLR8-specific inhibitors, mediated by L lactis G121 RNA,

261 s, but not the compounds that activated only TLR8, stimulated mouse immune cells in vitro and in vivo

262 Furthermore, TLR7 or TLR8 stimulation, independent of HCV, caused monocyte di

263 monocytes with a higher response to TLR4 and TLR8 stimulations in obesity.

264 TX-294 was approximately 100x more active on TLR8- than TLR7-transfected HEK cells (EC50, approximate

265 The murine TLR8 that does not respond to any known human TLR8 agoni

266 n showed antagonistic activities at TLR7 and TLR8; the C2 dimer with a propylene spacer was maximally

267 scription of TLR3, bditTLR4, TLR5, bditTLR7, TLR8, TLR9, and TLR10 upon Abeta stimulation is severely

268 degradation is extended to TLR3, TLR6, TLR7, TLR8, TLR9, and TLR10, whereas the cellular level of TLR

269 ubiquitous kinase, IRAK1, TLR1, TLR4, TLR6, TLR8, TLR9, and TNFR-associated factor 6) were downregul

270 cross-talk between ODNs, IRMs, and TLR7 and TLR8 uncovered by this study may have practical implicat

271 Finding that Toll-like receptor 8 (TLR8) was one of the proteins ubiquitinylated only in mu

272 Toll-like receptor 8 (TLR8) was required for inducing pro-IL-1beta expression,

273 Seven previously AR-associated SNPs from TLR8 were analyzed for AR associations in 422 AR patient

274 Six SNPs of TLR3, TLR7, and TLR8 were genotyped to determine their associations with

275 TLR7 and TLR8 were identified as eliciting antiviral effects when

276 his study TLR agonists selective for TLR7 or TLR8 were used to determine the repertoire of human inna

277 lated monocytes is greater for TLR2 than for TLR8, whereas expression of both TLRs increases signific

278 at live Bb induces transcription of TLR2 and TLR8, whereas IRS957 interferes with their transcription