ライフサイエンスコーパス: TLR7

1 ular Y. pestis by host Toll-like receptor 7 (TLR7).

2 ation threshold of potentially self-reactive TLR7.

3 beta, GBS induced TNF-alpha independently of TLR7.

4 to prevent unintended immune suppression of TLR7.

5 ss-of-function variants of the X-chromosomal TLR7.

6 with another nucleic acid-sensing receptor, TLR7.

7 in recipient cells and to activate endosomal TLR7.

8 mmunosuppressive activities of 2'OMe ASOs on TLR7.

9 RNA half molecules as abundant activators of TLR7.

10 ng from inappropriate activation of TLR9 and TLR7.

11 duction and autoimmune kidney disease in the Tlr7.1 transgenic mouse model of SLE.

12 e mice a Western diet or by applying topical TLR7/8 (Toll-like receptor) agonists.

13 We observed that TLR7/8 activation leads to a furin-dependent proteolytic

14 Therapeutic approaches aimed at blocking TLR7/8 activation would be predicted to increase phagocy

15 triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spared the polyinosin

16 gradation of the vesicles and release of the TLR7/8 agonist in native form after endocytosis, which r

17 Structure-based optimization of a dual TLR7/8 agonist led to the identification of the selectiv

18 We demonstrate that TLR7/8 agonist R848 induces anti-tumor responses and att

19 An exception is the TLR7/8 agonist R848, which can boost gastrointestinal an

20 mer-prodrug conjugate of an imidazoquinoline TLR7/8 agonist that in aqueous medium forms vesicular st

21 n of a small-molecule imidazoquinoline-based TLR7/8 agonist to 50-nm-sized degradable polymeric nanog

22 orm also enables PD-1-targeted delivery of a TLR7/8 agonist to the tumor microenvironment, increasing

23 hetic TLR4 agonist, and UM-3004, a lipidated TLR7/8 agonist, within the liposomal bilayer in order to

24 fect on NFkappaB activation in response to a TLR7/8 agonist.

25 e immunomodulators, such as imidazoquinoline TLR7/8 agonists for vaccine design and cancer immunother

26 were immunized with NPs containing TLR4 and TLR7/8 agonists mixed with soluble recombinant SIVmac239

27 that co-encapsulation of TLR4 and lipidated TLR7/8 agonists within the liposomal bilayer leads to in

28 a TLR7 sequence alignment to achieve a dual TLR7/8 antagonism profile and (ii) introduction of a flu

29 ntification of a highly potent and selective TLR7/8 antagonist (27) with in vivo efficacy.

30 d its application for hit generation of dual TLR7/8 antagonists are reported.

31 We identified TLR7/8 as mediators of monocyte differentiation and M2 M

32 Consequently, TLR7/8 biology in vivo must differ significantly from th

33 ges, but not by monocytes and DCs, through a TLR7/8 dependent mechanism; this leads to chloroquine se

34 specific for Toll-like receptor 4 (TLR4) and TLR7/8 encapsulated in poly(lactic-co-glycolic) acid (PL

35 d patients, we found increased expression of TLR7/8 in circulating monocytes that was associated with

36 ogels the potency of the agonist to activate TLR7/8 in in vitro cultured dendritic cells is largely r

37 nuated this expression, suggesting roles for TLR7/8 in induction of fibrocytes in HCV infection.

38 h1 cells or with IFNgamma, IL-2, anti-Ig and TLR7/8 ligand and that IL-21 dependent ASC formation is

39 -containing ICs induce calcium flux, whereas TLR7/8 ligand R848 do not.

40 Combinations of co-delivered TLR4 and TLR7/8 ligands have been demonstrated to have synergisti

41 er, we demonstrated that HCV ssRNA and other TLR7/8 ligands promote MPhi polarization and generation

42 ASC development by synergizing with IL-2 and TLR7/8 ligands to induce genome-wide epigenetic reprogra

43 After engagement of TLR7/8 or TLR9, BCMA was detected also on the cell surfa

44 n via Macrophage-inducible C-type lectin and TLR7/8 representing a novel approach to enhance the effi

45 Following TLR7/8 stimulation by its agonist R848, chemical inhibit

46 on strategies should target the induction of TLR7/8 stimulation in APCs in order to establish potent

47 stimulated monocytes while not doing so upon TLR7/8 stimulation.

48 The toll-like receptor 7 and 8 (TLR7/8) agonist Resiquimod (R848) has been recognized as

49 imod (R848) is a toll-like receptor 7 and 8 (TLR7/8) agonist with potent antitumor and immunostimulat

50 ion of three TLR pathways (TLR4, TLR1/2, and TLR7/8) or infection with influenza A virus.

51 g activities on Toll-Like Receptors 7 and 8 (TLR7/8), leading to divergent suppression of TLR7 and ac

52 s were analyzed after stimulation with TLR4, TLR7/8, and retinoic acid-inducible gene I agonists.

53 TLR7/8-activated neutrophils promoted cleavage of FcgRII

54 D86, and MHC class I in response to TLR3 and TLR7/8-agonists.

55 e IL6 from tumor-associated macrophages in a TLR7/8-dependent manner, which in turn promoted liposarc

56 ggesting it may act through a combination of TLR7/8/9 and ERK signaling mechanisms.

57 roquine (HCQ), a small molecule inhibitor of TLR7/8/9, following injury reduced NET formation, IL-10,

58 recapitulated by the simultaneous absence of TLR7, 9, and 13 but not by the absence of individual TLR

59 eptor (TLR) escort protein UNC93B, endosomal TLR7, -9, and -13, and cell surface TLR2 in MHV68 detect

60 m those induced by the viral sensors TLR3 or TLR7-9.

61 ntially decreases IFN-alpha production after TLR7/9 activation with different types of CpG oligodeoxy

62 ular immune complex deposition, and modulate TLR7/9 cytokine production in female MRL/lpr mice.

63 indicator for caution in clinical trials of TLR7/9 inhibitors for MYD88(L265P) B-cell malignancies.

64 and pro-inflammatory cytokines stimulated by TLR7/9 ligands.

65 ers, kidney disease, and response to in vivo TLR7/9 pathogenic signals.

66 as part of the Toll-like receptor-7 and -9 (TLR7/9) innate immune signaling pathways.

67 ow that the CXORF21 protein colocalises with TLR7, a pathway implicated in SLE pathogenesis.

68 Prenatal TLR7-activated mice have normal baseline locomotor activ

69 ovides a mechanism for dynamic regulation of TLR7 activation and signalling.

70 TLR7 activation by PapMV in the absence of C3 induced hi

71 microglial markers, indicates that prenatal TLR7 activation induces differential expression of hundr

72 Prenatal TLR7 activation via administration of the selective agon

73 lating the production of IFN-alpha following TLR7 activation.

74 we demonstrate here that a combined TLR4 and TLR7 adjuvant signals via the appropriate receptors and

75 sly reported that SLE neutrophils exposed to TLR7 agonist autoantibodies release interferogenic DNA,

76 In this study, we show that the selective TLR7 agonist GS-9620 induced HIV in peripheral blood mon

77 Using a murine model of psoriasis induced by TLR7 agonist imiquimod (IMQ), we show that VISTA deficie

78 F7, IFNB1, and ISG15 on stimulation with the TLR7 agonist imiquimod as compared with family members a

79 ion induced by topical administration of the TLR7 agonist imiquimod.

80 by injecting IL-23 or by application of the TLR7 agonist imiquimod.

81 GSK2245035 is a novel selective TLR7 agonist in pharmaceutical development.

82 C-2 that could make a potent purine scaffold TLR7 agonist to lose agonism and acquire antagonist acti

83 Delivery of a folate-targeted TLR7 agonist to these cells (i) reduced their immunosupp

84 mice were injected with viral (Imiquimod, a TLR7 agonist) or bacterial (ODN 2395, a TLR9 agonist) su

85 Here, we show that a highly selective TLR7 agonist, GS-9620, activated HIV from peripheral blo

86 be boosted in aged mice by treatment with a TLR7 agonist.

87 ice topically with the Toll-like receptor 7 (TLR7) agonist imiquimod (IMQ) to activate IFN-sensitive

88 ed IFN-alpha or TNF-alpha in response to the TLR7 agonists imiquimod and Sendai virus and to the TLR9

89 The TLR7 agonists R-837 and R-848 were used to mimic a viral

90 fied as a new series of potent and selective TLR7 agonists.

91 We also show that R-DOTAP stimulates both TLR7 and 9.

92 TLR7/8), leading to divergent suppression of TLR7 and activation of TLR8, in a sequence-dependent man

93 o C3 release from platelets as a function of TLR7 and C3 leads to neutrophil-DNA release and aggregat

94 development with subsequent upregulation of Tlr7 and Ifna1 Together, these data suggest that T1 B ce

95 , mediated through CD21, triggered endosomal TLR7 and led to the secretion of interferon (IFN) alpha

96 Why TLR9 represses disease while TLR7 and MyD88 have the opposite effect remains undefine

97 asmacytoid dendritic cells and monocytes via TLR7 and MyD88 signaling to protect from alphavirus diss

98 While RNA NANPs trigger both TLR7 and RIG-I mediated cytokine and interferon producti

99 demonstrate that simultaneous engagement of TLR7 and RIG-I pathways using particulate carriers is a

100 Inappropriate activation of endosomal TLR7 and TLR8 occurs in several autoimmune diseases, in

101 r work demonstrates that in human monocytes, TLR7 and TLR8 triggered different signaling pathways tha

102 -29a binds and activates dendritic cells via TLR7 and TLR8, resulting in the activation of the NF-kap

103 A virus specific and differentially involved TLR7 and TLR8, which sense single-stranded RNA.

104 gative regulation that differentiate between TLR7 and TLR9 are unknown.

105 Our data show that UNC93B-dependent TLR7 and TLR9 cooperate in and contribute to detection a

106 For example, TLR7 and TLR9 have opposing effects in mouse models of s

107 d VCAM and the pattern-recognition receptors TLR7 and TLR9 in the vascular wall, resulting in profoun

108 criptional program, robust responsiveness to TLR7 and TLR9 ligands, and a propensity for IgG2a/c prod

109 Our findings uncover a mechanism by which TLR7 and TLR9 specify monocyte fate and identify a speci

110 o produce type I IFNs (IFN-I) in response to TLR7 and TLR9 stimulation, it is assumed that their main

111 tic cells (pDC) in response to engagement of TLR7 and TLR9 with endocytosed nucleic acids.

112 o the IFN-alpha response to MHV68 in pDC are TLR7 and TLR9, but the contribution of TLR7 is masked by

113 bers of the Toll-like receptor (TLR) family, TLR7 and TLR9, can recognize self-RNA and self-DNA, resp

114 lls as well as expression of endosomal TLRs, TLR7 and TLR9, that modulate production of IFN.

115 fusion, and initiated signaling through both TLR7 and TLR9, which was not utilized in the absence of

116 injection of TLR9 agonist, and BCAP promoted TLR7 and TLR9-induced IFN-alpha production specifically

117 nt (Apoe (-/-)) mice and produced Apoe (-/-) Tlr7 (-/-) and Apoe (-/-) Tlr7 (+/+) littermates, follow

118 ted WT, Unc93b (-/-), Tlr7 (-/-) Tlr9 (-/-), Tlr7 (-/-), and Tlr9 (-/-) splenocytes.

119 5 acting downstream of Toll-like receptor 7 (TLR7) and, possibly, retinoic acid-inducible gene I (RIG

120 differentiation that appears independent of TLR7, and they provide a preclinical indicator for cauti

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

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

123 ulation of the Toll-like receptors (TLRs) 3, TLR7, and TLR9.

124 rent TLR agonists, including those for TLR2, TLR7, and TLR9.

125 Lastly, BMS-986126 inhibited TLR7- and TLR9-dependent responses using cells derived f

126 d chemokines in an FcgammaRIIA-dependent and TLR7- and TLR9-independent manner that likely contribute

127 rated synergy with prednisolone in assays of TLR7- and TLR9-induced IFN target gene expression using

128 arget in myriad autoimmune disorders, but no TLR7 antagonist is available for clinical use to date.

129 A TLR7 antagonist may mitigate atherosclerosis.

130 med by a comparative ligand-docking study in TLR7 antagonist pocket.

131 We ended up developing a clinically relevant TLR7 antagonist with favorable pharmacokinetics and 70.8

132 in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the same in TLR3- or Trif-

133 Herein, we report a purine scaffold TLR7 antagonist, first-of-its-kind to our knowledge, whi

134 date the in vivo applicability of this novel TLR7 antagonist, we demonstrated its excellent efficacy

135 ne series (10a and 10b) are potent selective TLR7 antagonists and may be considered as promising star

136 Moreover, the TLR7 antagonists depicted excellent selectivity against

137 Several of them are shown to be selective TLR7 antagonists without any TLR7 or TLR8 agonistic acti

138 n together, our data support the use of Alum-TLR7 as adjuvant for glycoconjugate vaccines.

139 abrogated emergence of infectious ERV in the Tlr7 (-/-) background.

140 difications abrogates RNA NANP activation of TLR7 but permits RIG-I dependent immune responses.

141 TLR7, but not TLR8, activation of monocytes also stimula

142 C93B1 that specifically limits signalling of TLR7, but not TLR9, and prevents TLR7-dependent autoimmu

143 gered by various TLRs (TLR2, TLR3, TLR4, and TLR7), C-type lectin receptors (Dectin-1, Dectin-2, and

144 Both UNC93B1 and TLR7 can be detected in exosomes, suggesting that recrui

145 Furthermore, like the type I IFN response, TLR7 contributed to the lethality of septicemic plague a

146 Therefore, TLR7 contributes to atherogenesis in Apoe (-/-) mice by

147 ter cell assays, we verified that potency at TLR7 correlates with IFN-alpha/beta production in human

148 TLR7 deficiency also reduced aortic arch SMC loss and le

149 However, TLR7 deficiency did not affect aortic wall elastin fragm

150 ion of TLR7 in atherosclerosis, we crossbred TLR7-deficient (Tlr7 (-/-)) mice with apolipoprotein E-d

151 ted in TLR9-deficient mice but attenuated in TLR7-deficient mice(1).

152 Although these effects were strictly TLR7 dependent, RNAdjuvant-mediated augmentation of vacc

153 Using Toll-like receptor 7 (TLR7)-dependent mouse models of systemic lupus erythemat

154 The induction of toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from

155 single autoreactive B cell clone drives the TLR7-dependent activation, expansion, and differentiatio

156 gnalling of TLR7, but not TLR9, and prevents TLR7-dependent autoimmunity in mice.

157 Notably, GBS induced a TLR7-dependent IFN-beta signal only in MPhi-like but not

158 TLR7-dependent inflammatory responses were differentiall

159 ediated knockdown found 43 regulators of the TLR7-dependent IRF5 signaling pathway.

160 rnal organs and 16S rDNA sequencing revealed TLR7-dependent translocation of L. reuteri in mice and f

161 When RABV invaded from the periphery, TLR7 detected viral single-stranded RNA and triggered im

162 eas TLR9 and TLR3 are released from UNC93B1, TLR7 does not dissociate from UNC93B1 in endosomes and i

163 blood cells develop in Toll-like receptor 7 (TLR7)-driven inflammation.

164 ules STAT1 and T-bet in B cells in promoting TLR7-driven AFC, GC, and SLE development whereas T1IFN s

165 peripheral B cells further demonstrates that TLR7-driven autoimmune AFC, GC and Tfh responses and SLE

166 B cell-intrinsic roles of STAT1 and T-bet in TLR7-driven GC, Tfh and plasma cell differentiation.

167 (IRF5), associated with MAS, participated in TLR7-driven iHPC differentiation.

168 eriments revealed NXF1 selectively regulates TLR7-driven IRF5 transcriptional activity, suggesting a

169 tor for PI3K (BCAP) promoted many aspects of TLR7-driven lupus-like disease, including Isg15 and Ifit

170 ing Y. pestis infection and suggest that the TLR7-driven type I IFN response plays an important role

171 nsequential early in life, while symptoms of TLR7 dysregulation take longer to manifest.

172 strated that when RABV invades into the CNS, TLR7 enhances the production of inflammatory cytokines w

173 cations include an increased accumulation of TLR7-expressing Ly6C(hi) inflammatory monocytes at the s

174 Increased TLR7 expression in human atherosclerotic lesions suggest

175 Here we demonstrated TLR7 expression in macrophages, smooth muscle cells (SMC

176 ages of pancreatic neoplasia, but epithelial Tlr7 expression is relatively uncommon.

177 g TLR8 sensing of Resiquimod, which preserve TLR7 function, and promote strong activation of phagocyt

178 While this immune response, triggered by TLR7, helped to clear viruses, it also increased neuroin

179 eated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists showed decreased proliferation

180 To test a direct participation of TLR7 in atherosclerosis, we crossbred TLR7-deficient (Tl

181 e present study, we investigated the role of TLR7 in the pathogenicity of RABV in a mouse model.

182 Mechanistically, TLR7 induced PI3K/mammalian target of rapamycin signalin

183 Using TLR7-induced and TLR7 overexpression models of SLE, we r

184 and deficient for IFN-gammaR indicates that TLR7-induced IFN-gamma activates multiple signaling path

185 reviously unrecognized indispensable role of TLR7-induced IFN-gamma signaling in promoting AFC and GC

186 per T (Tfh) cells are the major producers of TLR7-induced IFN-gamma.

187 lation and tissue inflammation in a model of TLR7-induced lupus.

188 strated its excellent efficacy in preventing TLR7-induced pathology in a preclinical murine model of

189 enin-1 by UNC93B1 facilitates the sorting of TLR7 into intralumenal vesicles of multivesicular bodies

190 vaccines in humans, we investigated if Alum-TLR7 is able to improve immunogenicity of this class of

191 Our results demonstrate that TLR7 is an innate recognition receptor for RABV, which r

192 dendritic cells (pDCs), we demonstrated that TLR7 is an innate recognition receptor for RABV.

193 TLR7 is associated with development of systemic lupus er

194 Previous studies have revealed that TLR7 is involved in the immune response to RABV.

195 C are TLR7 and TLR9, but the contribution of TLR7 is masked by the presence of TLR9.

196 udies revealed that stromal, not neoplastic, TLR7 is requisite for R848-mediated responses.

197 In patient samples, we found Tlr7 is ubiquitously expressed in stroma across all stag

198 Toll-like receptor 7 (TLR7) is an established therapeutic target in myriad aut

199 tudy demonstrated that Toll-like receptor 7 (TLR7) is essential in the induction of anti-RABV antibod

200 Activation of TLR7 leads to the production of several stimulatory cyto

201 n RABV had invaded the CNS, its detection by TLR7 led to the production of cytokines and chemokines a

202 Stimulation with TLR7 ligand enhances formation of IRF5-NXF1 protein comp

203 studies demonstrate that treatment with the TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, re

204 TLR7 ligand imiquimod treated IFN-gamma reporter mice sh

205 XCL1, and IL-6 when stimulated in vitro with TLR7 ligand.

206 ation of the FOXO3A pathway, TLR3, TLR4, and TLR7 ligands activated FOXO3A as indicated by decreased

207 eral dose combinations of synthetic TLR4 and TLR7 ligands are potent adjuvants for recombinant influe

208 Combining the TLR4 and TLR7 ligands balances Th1 and Th2-type immune responses

209 antiproliferative effects of TLR3, TLR4, and TLR7 ligands correlated with significant downregulation

210 all-molecule Toll-like receptor 4 (TLR4) and TLR7 ligands is a potent adjuvant for recombinant influe

211 In this study, we show that TLR2 and TLR7 ligands potently lower the Ag threshold for cytokin

212 hat murine CD8(+) T cells can sense TLR2 and TLR7 ligands, resulting in rapid production of IFN-gamma

213 roduced Apoe (-/-) Tlr7 (-/-) and Apoe (-/-) Tlr7 (+/+) littermates, followed by feeding them an athe

214 amma signaling in differential regulation of TLR7-mediated Ab-forming cell (AFC) and germinal center

215 n of IRAK4 repressed SLE immune complex- and TLR7-mediated activation of human plasmacytoid dendritic

216 TLR2-, but not TLR7-mediated costimulation, can enhance mRNA stability

217 Both IRAK4 and BTK inhibition reduced the TLR7-mediated differentiation of human memory B cells in

218 Unlike TLR7-mediated disease, which requires type I interferon

219 lation of STAT3 signaling is responsible for TLR7-mediated inhibition of Th17 cells due to induction

220 (DCs), as well as both B cells and DCs, in a TLR7-mediated model of autoimmunity, similar to systemic

221 and identify the critical role of B cells in TLR7-mediated resistance to bacterial infection.

222 TLR7-mediated suppression of Th17 cells does not require

223 Toll-like receptor 7 (TLR7) mediates autoantigen and viral RNA-induced cytokin

224 Compared to Apoe (-/-) Tlr7 (+/+) mice, Apoe (-/-) Tlr7 (-/-) mice showed reduc

225 Reduced atherosclerosis in Apoe (-/-) Tlr7 (-/-) mice did not affect lesion macrophage-positiv

226 ed to Apoe (-/-) Tlr7 (+/+) mice, Apoe (-/-) Tlr7 (-/-) mice showed reduced aortic arch and sinus les

227 ERV reactivation in Tlr7 (-/-) mice was comparable in the presence or absenc

228 ected in the plasma of hA3G(+) Apobec3 (-/-) Tlr7 (-/-) mice, and infectious ERV virions could not be

229 of replication-competent, infectious ERV in Tlr7 (-/-) mice.

230 therosclerosis, we crossbred TLR7-deficient (Tlr7 (-/-)) mice with apolipoprotein E-deficient (Apoe (

231 ession on normal IMC; IMC from Tlr2(-/-) and Tlr7(-/-) mice demonstrated similar results, although to

232 ation, which was significantly attenuated in TLR7(-/-) mice.

233 Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically pr

234 Alteration of the microbiome alters TLR7-MyD88 signaling in plasmacytoid dendritic cells (pD

235 opposing effects of TLR9 and TLR3, TLR4, and TLR7 on the key angiogenic pathways, Fli1 and FOXO3A.

236 oduction was abolished in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the

237 to be selective TLR7 antagonists without any TLR7 or TLR8 agonistic activity.

238 These compounds have been tested for their TLR7 or TLR8 agonistic and antagonistic activities.

239 erentiation into MPhis could be prevented by TLR7 or TLR8 knockdown.

240 Furthermore, TLR7 or TLR8 stimulation, independent of HCV, caused mon

241 transcriptional signature, and they rely on TLR7 or TLR9 signals in the context of Th1 cytokines for

242 heterodimer (referred to herein as TLR1/2), TLR7 or TLR9, but not upon engagement of TLR3 or TLR4.

243 We found that deleting TLR7 or TLR9, the receptors for RNA and DNA, had no effe

244 /-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were more susceptible to P. a

245 generated Mer(-/-) mice with a global MyD88, TLR7, or TLR9 deficiency and cell type-specific MyD88 de

246 sponsible for anemia and thrombocytopenia in TLR7-overexpressing mice, which have a macrophage activa

247 Using TLR7-induced and TLR7 overexpression models of SLE, we report in this stu

248 n monocytes exposed to HCV, and knockdown of TLR7 partially attenuated this expression, suggesting ro

249 Tlr7 (-/-) pDC responded similarly to WT.

250 ates multiple signaling pathways to regulate TLR7-promoted SLE.

251 Here, we establish that TLR7 recognizes RABV and facilitates the production of s

252 Although endosomal TLR7 recognizes single-stranded RNAs, their endogenous R

253 FN-beta is required for optimal survival and TLR7 responses of transitional B cells in the spleen and

254 to periodontitis was observed in carriers of TLR7-rs3853839 (CC versus GG and CG, P = 0.02, OR 0.30,

255 tion between TLR1-rs5743611, TLR4-rs7873784, TLR7-rs3853839, and TLR8-rs3764879 and susceptibility to

256 ism (IL-12p40 EC(50) = 220 nM) and >100-fold TLR7 selectivity (IFN-alpha EC(50) > 50 muM) was observe

257 ction in bumble mice was dependent on intact TLR7 sensing and IFN-I signaling within B-1 cells.

258 re we demonstrate that Toll-like receptor 7 (TLR7) sensing and type I interferon (IFN-I) signaling in

259 timization were (i) a core morph guided by a TLR7 sequence alignment to achieve a dual TLR7/8 antagon

260 In addition, we show that TLR7 signaling can suppress Th1 cell development and fun

261 TLR7 signaling caused the development of inflammatory he

262 s article, we demonstrate that activation of TLR7 signaling in T cells can inhibit Th17 cell differen

263 Enhanced TLR7 signaling in Vsir (-/-) dendritic cells (DCs) led t

264 her, these data demonstrate that an atypical TLR7 signaling pathway contributes to type I IFN express

265 Furthermore, we found that TLR7 signaling specifically increased expression of the

266 combined adjuvant is dependent upon TLR4 and TLR7 signaling via myeloid differentiation primary respo

267 tivates endosomal NOX2 oxidase and restricts TLR7 signaling, and that an endosomal NOX2 inhibitor dec

268 und that HIV-induced IFN production required TLR7 signaling, receptor-mediated entry, fusion, and vir

269 trategy to manipulate Th17/Th1 cells through TLR7 signaling, with important implications for successf

270 e production and leukocyte migration through TLR7 signaling.

271 Mutations in UNC93B1 that lead to enhanced TLR7 signalling also disrupt binding of UNC93B1 to synte

272 TLR7 specificity is confirmed in murine models lacking t

273 At the same time, TLR7 stimulation in the absence of functional Notch2 sig

274 MNECs, and HNECs within 15 minutes of local TLR7 stimulation.

275 ed dysregulated responses to TLR4, TLR8, and TLR7 stimulation.

276 madelta(+) and CD4(+) Th17 T cells following TLR7 stimulation.

277 Toll-like receptor 7 (TLR7) stimulation in the airways may reduce responses to

278 hich is the only known signaling adaptor for TLR7, suggesting that a noncanonical mechanism occurs in

279 y dissecting the structural requirements for TLR7-targeted activity for a purine scaffold.

280 nocyte-specific pattern recognition receptor TLR7, the Langerhans cell chemoattractant CCL20, and pro

281 ws that TASL is an innate immune adaptor for TLR7, TLR8 and TLR9 signalling, revealing a clear mechan

282 es TRAILshort production are type I IFNs and TLR7, TLR8, and TLR9 agonists.

283 4-diamine was found to be a very potent dual TLR7/TLR8 agonist.

284 Dual TLR7/TLR8 agonists markedly upregulate CD80 expression i

285 In an effort to identify novel dual TLR7/TLR8-active compounds, we undertook structure-activ

286 ound that in Unc93b (-/-) pDC, as well as in Tlr7 (-/-) Tlr9 (-/-) double-knockout pDC, the IFN-alpha

287 ficient mice, and in the liver and spleen of Tlr7 (-/-) Tlr9 (-/-) mice.

288 on and latent viral loads, particularly from Tlr7 (-/-) Tlr9 (-/-) splenocytes compared to levels in

289 V68 from latently infected WT, Unc93b (-/-), Tlr7 (-/-) Tlr9 (-/-), Tlr7 (-/-), and Tlr9 (-/-) spleno

290 ple adjuvant combination, TLR4/TLR9 and TLR4/TLR7/TLR9, for further evaluation and found that both co

291 t of TLR2 (Toll-like receptor 2)-engaged and TLR7 (Toll-like receptor 7)/TLR8 (Toll-like receptor 8)-

292 In mice deficient for Toll-like receptor 7 (TLR7), transcribed ERV loci can recombine and generate i

293 etween the beneficial and harmful effects of TLR7-triggered immune responses.

294 In the murine plague model, TLR7 was a significant contributor to the expression of

295 In contrast, TLR7 was important for defense against disease in the lu

296 otably, mortality in the absence of Mavs and Tlr7 was independent of viral load or MyD88-dependent si

297 e loss-of-function variants of X-chromosomal TLR7 were identified that were associated with impaired

298 terize the effects of prenatal activation of TLR7, which is implicated in the pathogenesis of autoimm

299 xpress high levels of TLR9 and low levels of TLR7, which may explain why TLR9 dysregulation is partic

300 ion of innate immunity through engagement of TLR7 with papaya mosaic virus (PapMV)-like nanoparticles