ライフサイエンスコーパス: TLR9

1 recognition receptor, Toll-like receptor 9 (TLR9).

2 to ligation of BCR and Toll-like receptor 9 (TLR9).

3 blocking BAFF, type I interferon, or TLR7 to TLR9.

4 n that generated a dominant-negative form of TLR9.

5 codon bias limit TLR7 expression relative to TLR9.

6 Ly6C(lo) monocytes after triggering TLR2 or TLR9.

7 nd that NK cell activation by PG545 requires TLR9.

8 mitochondria and has the ability to activate TLR9.

9 models of SLE and is negatively regulated by TLR9.

10 is critical for trafficking and cleavage of TLR9.

11 imulation with ligands that activate TLR7 or TLR9.

12 wo independent cleavage events that regulate TLR9.

13 romosome 9, we identify a putative modifier, TLR9.

14 sine dinucleotide) motifs activate endosomal TLR9.

15 perties of ODNs modulate their activation of TLR9.

16 Here we show that DNase II is required for TLR9.

17 gnificant loss of the propensity to activate TLR9.

18 of DNase II in endolysosomal DNA sensing by TLR9.

19 gonists, including those for TLR2, TLR7, and TLR9.

20 TLR9(1-440) coimmunoprecipitates with full-length TLR9 a

21 by coexpression of the N-terminal fragment (TLR9(1-440)), inclusion of the hinge region (TLR9(441-10

22 indings were a protective association of the TLR9 +2848 GG genotype and a risk-enhancing association

23 ion showed a trend toward protection for the TLR9 +2848 GG genotype.

24 TLR9(1-440)), inclusion of the hinge region (TLR9(441-1032)), or overexpression of UNC93B1, the last

25 immunoprecipitates with full-length TLR9 and TLR9(471-1032) but does not rescue the native glycosylat

26 Lastly, we show that TLR9(471-1032) is also a dominant-negative regulator of

27 nappropriate trafficking likely explains why TLR9(471-1032) is nonfunctional.

28 s to generate a mature form of the receptor (TLR9(471-1032)).

29 We show that TLR9(471-1032), corresponding to the proteolytically cle

30 toprotective phenotype otherwise observed in TLR9 absence.

31 TLR9 accumulates on the cell surface, where it recognize

32 nhibition of phagosomal acidification blocks TLR9 accumulation on phagosomes containing beta-1,3 gluc

33 TLR9-activated PSCs mediate their protumorigenic effects

34 emonstrate that levels of H. pylori-mediated TLR9 activation and expression are directly related to g

35 i cancer-associated cag T4SS is required for TLR9 activation and that H. pylori DNA is actively trans

36 we demonstrate that DNase II is required for TLR9 activation by bacterial genomic DNA.

37 Specifically, TLR9 activation can induce proinflammatory signaling in

38 plasma resulted in a substantial decrease in TLR9 activation capacity.

39 as well as BTK deficiency, also resulted in TLR9 activation defects in B cells similar to those in p

40 TLR9 activation depends on both the inter-DNA spacing an

41 We show that TLR9 activation has distinct effects on the epithelial,

42 cellular compartments for the early steps of TLR9 activation in dendritic cells (DCs).

43 activate TLR9 directly but instead enhances TLR9 activation through the elevation of the TLR9 ligand

44 N requires backbone phosphorothioate but not TLR9 activation to render and maintain endothelial stalk

45 These results indicate that TLR9 activation via the cag island may modify the risk f

46 identify the sequence properties that govern TLR9 activation.

47 ated degradation of self-DNA is required for TLR9 activation.

48 ne pDCs did not express BCMA, not even after TLR9 activation.

49 thymic B cells using Epstein-Barr virus and TLR9 activation.

50 ative AML, BTK couples Toll-like receptor 9 (TLR9) activation to nuclear factor kappaBeta and STAT5.

51 ation of T1D mice with a CpG oligonucleotide TLR9 agonist (ODN 1585) enhances expansion of IL-22-prod

52 onists imiquimod and Sendai virus and to the TLR9 agonist CpG.

53 ly increased and was further enhanced by the TLR9 agonist CpGB.

54 receptor (TLR) agonists in vivo In mice, the TLR9 agonist cytosine-phosphate-guanine (CpG) oligodeoxy

55 nd human B cells, BCR ligands that deliver a TLR9 agonist induce an initial proliferative burst that

56 Whereas treatment with a TLR9 agonist protected IgH V region unmutated, but not m

57 h enhanced innate signaling, we used TLR4 or TLR9 agonist treatment at the time of infection, which r

58 TLR9 agonist treatment in HIV infection has a dual poten

59 When compared with CpG (TLR9 agonist), beta-glucan-activated cells secreted sign

60 gonist, polyinosinic-polycytidylic acid, and TLR9 agonist, CpG, reduced tumor growth in all tumor mod

61 ast phenotype driven by stimulation with the TLR9 agonist, CpG-DNA.

62 tumoral injection of a highly interferogenic TLR9 agonist, SD-101, in anti-PD-1 nonresponders led to

63 ligand (CD40L) and the Toll-like receptor 9 (TLR9) agonist cytidine-phosphate-guanosine oligodeoxynuc

64 drug molecule-a novel Toll-like receptor 9 (TLR9) agonist, MGN1703-could function as an enhancer of

65 tion of Toll-like receptor 2/6 (TLR 2/6) and TLR9 agonists (Pam2-ODN) induces protective mucosal defe

66 ISCOMATRIX vaccines combined with TLR3 and TLR9 agonists represent a promising cancer immunotherapy

67 ependently of TLR agonist used (i.e. TLR2 or TLR9 agonists).

68 proliferation induced by synthetic TLR7 and TLR9 agonists, as well as TLR agonist-induced costimulat

69 Here we used synthetic TLR9 agonists, cytosine-phosphate-guanosine oligodeoxynu

70 ker responses were evident after exposure to TLR9 agonists, potentially due to very low expression of

71 oduction are type I IFNs and TLR7, TLR8, and TLR9 agonists.

72 Of note, the expression of Tlr9, Aim2 and Tmem173, key DNA sensor genes, was marked

73 s triggered by Brucella abortus DNA involves TLR9, AIM2, and stimulator of IFN genes (STING).

74 te DNA-sensing through Toll-like receptor 9 (TLR9) along with inflammatory cytokine receptor IFN-gamm

75 Variations in TLR9 and IL10 are associated with the outcome of H. ducr

76 Both TLR9 and its ligand, the dinucleotide CpG, were present

77 ATRA-treated cGVHD B cells had elevated TLR9 and PAX5, but not BLIMP1 (a gene-expression pattern

78 of B cells via the innate immunity receptors TLR9 and RP105.

79 inhibited the expression of TLR4, TLR5, and TLR9 and their downstream cytokine signaling in the ging

80 s detected by pattern-recognition receptors (TLR9 and TLR3) leading to a type-I IFN mediated innate i

81 This work revealed opposing effects of TLR9 and TLR3, TLR4, and TLR7 on the key angiogenic path

82 dual and a triple adjuvant combination, TLR4/TLR9 and TLR4/TLR7/TLR9, for further evaluation and foun

83 Unc93b1(3d/3d) mutation, which blocks TLR9 and TLR7 signaling, or Tlr9 deficiency suppressed M

84 1-440) coimmunoprecipitates with full-length TLR9 and TLR9(471-1032) but does not rescue the native g

85 uch as endosomal TLRs (TLR3, TLR7, TLR8, and TLR9) and cytoplasmic proteins (absent in melanoma 2 and

86 endolysosome, can be immunoprecipitated with TLR9, and binds to CpG intracellulary.

87 propose that this mechanism integrating BCR, TLR9, and cytokine signals provides a peripheral checkpo

88 elationship among the B cell receptor (BCR), TLR9, and cytokine signals that regulate B cell response

89 TLR9, establish the cellular requirement for TLR9, and evaluate the role of obesity-induced changes i

90 Finally, our data have suggested that TLR2, TLR9, and Mal/TIRAP controlled differentially the emerge

91 AC recognition receptors, low expression of TLR9, and reduced TLR responsiveness to nucleic acids.

92 xpressing cells, and a clinically applicable TLR9 antagonist blocked the development of NASH when giv

93 This effect was negated by either a TLR9 antagonist or DNase treatment.

94 Both NO and TLR9 are important elements of innate immunity to mycoba

95 in CD4(+) T cells, NA-TLRs, TLR3, TLR8, and TLR9 are upregulated by FcgammaRIIIa-pSyk cosignaling an

96 autoreactivity-associated locus and validate Tlr9 as a candidate gene within the locus.

97 lasma membrane and associated with disrupted TLR9 at the submembrane.

98 by strength of TLR9 signal, because stronger TLR9(B6) signals, but not weaker TLR9(BALB/c) signals, n

99 se stronger TLR9(B6) signals, but not weaker TLR9(BALB/c) signals, negatively regulate CD45E613R B ce

100 TMPD-injected Tlr9(-/-) BALB/c mice develop higher autoantibody titers

101 We now show that Tlr9(-/-) BALB/c mice injected i.p. with TMPD develop mo

102 After engagement of TLR7/8 or TLR9, BCMA was detected also on the cell surface of pDCs

103 The TLR7 to TLR9 blocker hydroxychloroquine has been in use in patie

104 Ex vivo, TLR9(-/-) bone marrow-derived macrophages produced more

105 entation and crosspriming depend not only on TLR9, but also on interferon type I signaling, and both

106 ent of NASH in animal models requires intact TLR9, but how the TLR9 pathway is activated in NASH is n

107 ate receptors, such as Toll-like receptor 9 (TLR9), can trigger inflammation.

108 ocalized to the kidney more efficiently than Tlr9(-/-) CD4(+)CD25(+) cells.

109 ned the ex vivo dose effects mediated by the TLR9(+) cell populations (dendritic cells, macrophages,

110 ared to the cytokine production in WT cells, TLR9(-/-) cells exhibited significantly decreased proinf

111 nificantly diminished cytokine production in TLR9(-/-) cells relative to the cytokine production in W

112 t AbISCO-100/Matrix-M (AbISCO), to assess if TLR9 co-stimulation would quantitatively or qualitativel

113 The minimal ODNs that activate human TLR9 comprise 2 CG dinucleotides separated by 6-10 nt, w

114 vestigated whether an N-terminal fragment of TLR9 could be responsible for regulation of the mature o

115 olyribocytidylic acid), TLR2 (Pam3CSK4), and TLR9 (CpG) remained comparable within the first 2 h.

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

117 on, which blocks TLR9 and TLR7 signaling, or Tlr9 deficiency suppressed MYD88(L265P) B-cell growth in

118 ins TLR9-dependent, as inhibition is lost in TLR9 deficient mice.

119 Toll-like receptor 9 (TLR9)-deficient (TLR9(-/-)) mice are resistant to period

120 Nevertheless, the corresponding TLR9-deficient autoimmune-prone strains consistently dev

121 TLR9-deficient mice responded significantly weaker to Id

122 ls from wild-type, Unc93b1(3d/3d)-mutant, or Tlr9-deficient mice were transduced with retrovirus enco

123 artery endothelial cell, wild-type mice, and TLR9-deficient mice.

124 deficient in CD4(+)CD25(+) cells, and WT and TLR9-deficient Tregs had similar suppressive function ex

125 on markedly accelerates oncogenesis, whereas TLR9 deletion is protective.

126 In addition, Dectin-1 regulates TLR9-dependent gene expression.

127 molecules, to activate B cells through a BCR/TLR9-dependent mechanism.

128 Lastly, BMS-986126 inhibited TLR7- and TLR9-dependent responses using cells derived from lupus

129 utrophils show impaired endosomal-initiated, TLR9-dependent signaling and deficient TLR9-specific CD1

130 ttenuation of angiogenesis, however, remains TLR9-dependent, as inhibition is lost in TLR9 deficient

131 oligonucleotide-based inhibitors of TLR7 to TLR9, despite showing promise in animal models of lupus,

132 nt affinities for CG are formed in the human TLR9 dimer, with a very stringent binding site interacti

133 We demonstrate that PG545 does not activate TLR9 directly but instead enhances TLR9 activation throu

134 Instead, TLR9-driven inflammation induced a Ccr2-independent expa

135 ated in peripherally inflamed tissues during TLR9-driven inflammation.

136 However, responses to TLR9 engagement are not uniform, but diametrically oppos

137 Toll-like receptor 9 (TLR9) enhances proinflammatory responses, but whether it

138 were to identify NASH-associated ligands for TLR9, establish the cellular requirement for TLR9, and e

139 ted the response of TLR2-, TLR3-, TLR4-, and TLR9-expressing HEK293 cells to stimulation with Pam3CSK

140 TLR3 and TLR9 expression and downstream MYD88 signalling molecule

141 IL-25 up-regulated TLR9 expression by pDCs and orchestrated the responses t

142 Results showed induction of TLR9 expression by TGF-beta in lung myofibroblasts and a

143 aled that emigrated neutrophils up-regulated TLR9 expression during acetaminophen-mediated necrosis,

144 modulates pDC function through an effect on TLR9 expression.

145 djuvant combination, TLR4/TLR9 and TLR4/TLR7/TLR9, for further evaluation and found that both combina

146 TLR7 and TLR9 function as innate sensors of viral infection as th

147 ught to analyze whether CD19 is required for TLR9 function in human B cells.

148 t of the CD45E613R mutation, manipulation of TLR9 gene dosage eliminates ANA in CD45E613R.BALB/c mice

149 DNA binding to neutrophils' surface (s)TLR9 has been evidenced.

150 Additionally, TLR9 has immune-suppressive effects in the tumor microen

151 Collectively, our work shows that TLR9 has protumorigenic effects in pancreatic carcinoma

152 We propose that synergistic TLR9/IFN-gammaR activation of T-bet(+) B cells is a mech

153 MyD88(-/-), TLR2(-/-), TLR3(-/-), TLR4(-/-), TLR9(-/-), IL-1R(-/-), and IL-18(-/-) mice, we found tha

154 and, for the first time, point to a role of TLR9 in AML.

155 s, potentially due to very low expression of TLR9 in bdMphi.

156 either uptake of GFP-HSV nor localization of TLR9 in CD71(+) endosomes, directing us to investigate d

157 mechanism that prevents hyper-activation of TLR9 in DCs.

158 the requirement for proteolytic cleavage of TLR9 in endosomes to generate a mature form of the recep

159 sponse to P. gingivalis, thereby implicating TLR9 in inflammatory responses to this organism.

160 ion and depletion studies defined a role for TLR9 in maintaining Treg-mediated homeostasis in cisplat

161 Validating a role for TLR9 in modifying autoreactivity in the context of the C

162 ly increased levels of TLR4 but not TLR2 and TLR9 in ONFH.

163 e, Semapimod causes accumulation of TLR4 and TLR9 in perinuclear space, consistent with endoplasmic r

164 otides (CpG-ODN), to investigate the role of TLR9 in vascular pathophysiology and identify potential

165 Activation of TLR9 in vivo exacerbated IPF in mice and induced differe

166 GB1) protein activates Toll-like receptor 9 (TLR9) in the adipose-recruited pDCs by transporting extr

167 ion, as highlighted by Toll-like receptor 9 (TLR9) in the endosomal compartment and cyclic GMP-AMP sy

168 lator of vascular homeostasis, Fli1, whereas TLR9 increased Fli1 levels.

169 CD19 is required for TLR9-induced B-cell activation.

170 Rolipram inhibited both TLR7/8- and TLR9-induced IFN regulatory factor 5 and NF-kB p65 nucle

171 rgy with prednisolone in assays of TLR7- and TLR9-induced IFN target gene expression using human PBMC

172 CSF-induced cDCs increased the expression of TLR9-induced IL-12p40 and IFN-beta, but not of IL-10.

173 signal transduction events that occur during TLR9-induced IRF7 activation.

174 demonstrate that ligation of TLR3, TLR4, and TLR9 induces murine DC production of complement componen

175 mechanisms and biological pathways by which TLR9 instigates periodontal inflammation are yet to be i

176 TLR9 is activated by sensing ligands in specific endosom

177 TLR9 is an endosomal TLR that also modulates the inflamm

178 TLR9 is an innate immune receptor important for recogniz

179 gle activation of the innate immune receptor TLR9 is sufficient to fully engage BCR signaling in ZAP-

180 We found that TLR9 is widely expressed early during the course of panc

181 Toll-like receptor 9 (TLR9) is an endosome bound, innate immune receptor that

182 ed receptors, Toll-like receptor (TLR) 7 and TLR9, is balanced to allow recognition of microbial nucl

183 Toll-like receptor 9 (TLR9), its adaptor MyD88, the downstream transcription f

184 In this study, we utilized TLR9 knockout (TLR9(-/-)) mice and wild-type (WT) contro

185 In contrast, the TLR9 ligand class C, ODN2395, increased angiogenesis.

186 TLR9 activation through the elevation of the TLR9 ligand CpG in DCs.

187 57BL/6 (B6) mice stimulated in vivo with the TLR9 ligand CpG, a strong type 1 IFN inducer.

188 ides insight into the molecular mechanism of TLR9 ligand recognition.

189 coll), each containing >100 molecules of the TLR9 ligand, DV230.

190 ted the ability of the Toll-like receptor 9 (TLR9) ligand CpG to modulate established disease in the

191 course of pancreatic transformation and that TLR9 ligands are ubiquitous within the tumor microenviro

192 TLR9 ligands normally induce phosphorylation of CD19 thr

193 l guanosyl dinucleotide motifs (CpG ODN) are TLR9 ligands with attractive immunostimulatory propertie

194 l program, robust responsiveness to TLR7 and TLR9 ligands, and a propensity for IgG2a/c production.

195 We test two types of TLR9 ligands, CpG-A and CpG-B, and show that only CpG-A

196 mounts of type I IFN in response to TLR7 and TLR9 ligands, whereas conventional DCs (cDCs) predominan

197 ood human B cells were stimulated by TLR7 or TLR9 ligands, with or without IFN-alpha, and compared wi

198 nfiltration in the WT ligated but not in the TLR9(-/-) ligated mice compared to the unligated control

199 Conversely, TLR9 ligation induces pancreatic stellate cells (PSCs) t

200 TLR9 ligation markedly accelerates oncogenesis, whereas

201 on by pDCs and orchestrated the responses to TLR9 ligation.

202 optimum spacing can interlock with multiple TLR9 like a zipper, leading to multivalent electrostatic

203 r for IgE, followed by Toll-like receptor 9 (TLR9)-mediated sensing of DNA in phagosomes.

204 jection or ablation of Toll-like receptor 9 (TLR9)-mediated sensing significantly reduced systemic in

205 tic regression and determined that defective TLR9-mediated activation of IDO1 induction is associated

206 P-70 appears to be of crucial importance for TLR9-mediated activation of Syk.

207 Mechanistically, TLR9-mediated antiapoptotic signals in ZAP-70-positive C

208 TLR9-mediated inflammation is also implicated in periodo

209 dentified the mechanism responsible for TLR7/TLR9-mediated neuronal apoptosis.

210 In addition, activation of TLR9-mediated NF-kappaB and MAPK and nuclear translocati

211 These results demonstrate that TLR9-mediated pathogen detection is important for host d

212 that cAMP-mediated signaling may abrogate a TLR9-mediated survival signal in prognostically unfavora

213 ce with the cell type-specific expression of TLR9, MGN1703 treatment led to pronounced activation of

214 of the infected WT mice but not in infected TLR9(-/-) mice compared to their levels in controls.

215 xperimental murine AKI induced by cisplatin, Tlr9(-/-) mice developed enhanced renal injury and exhib

216 In a murine model of A. baumannii pneumonia, TLR9(-/-) mice exhibit significantly increased bacterial

217 model of periodontitis, we demonstrate that TLR9(-/-) mice exhibited significantly less alveolar bon

218 Following systemic A. baumannii infection, TLR9(-/-) mice have significantly increased bacterial bu

219 riodontitis, revealed reduced neutrophils in TLR9(-/-) mice on day 1 postinfection compared to the le

220 doptive transfer of wild-type neutrophils to TLR9(-/-) mice reversed the hepatoprotective phenotype o

221 Tlr9(-/-) mice were not deficient in CD4(+)CD25(+) cells

222 y CD25(-) splenocytes from wild-type (WT) or Tlr9(-/-) mice, AKI was similarly enhanced.

223 The TMP-injected Tlr9(-/-) mice, and not the wild-type mice, also develop

224 m-infected WT mice or P. gingivalis-infected TLR9(-/-) mice, which were resistant to bone loss.

225 duced on peripheral CD4(+)CD25(+) cells from Tlr9(-/-) mice.

226 In this study, we utilized TLR9 knockout (TLR9(-/-)) mice and wild-type (WT) controls in a murine

227 Toll-like receptor 9 (TLR9)-deficient (TLR9(-/-)) mice are resistant to periodontitis, a diseas

228 We conclude that TLR9 modulates periodontal disease progression at both t

229 ative regulator of TLR signaling, in ligated TLR9(-/-) mouse gingival tissues compared to its express

230 dy, we report that the Toll-like receptor 9 (TLR9)-MyD88 pattern-recognition receptor pathway is uniq

231 e showed that after infection with ECTV, the TLR9-MyD88-IRF7 pathway was necessary in CD11c(+) cells

232 acted to extracellular DNA by activating the TLR9/NF-kappaB pathway.

233 Activation of TLR9 occurs through a contact-dependent mechanism betwee

234 ment in response to a high-fat diet required TLR9 on lysozyme-expressing cells, and a clinically appl

235 an unexpected, powerful inhibitory effect of TLR9 on MYD88(L265P) B-cell proliferation and differenti

236 gene expression level of TLR2 (P = .02) and TLR9 (P = .02), a greater than 4-fold increase in IL-17A

237 luate the role of obesity-induced changes in TLR9 pathway activation.

238 mal models requires intact TLR9, but how the TLR9 pathway is activated in NASH is not clear.

239 hese data demonstrate that activation of the TLR9 pathway provides a link between the key metabolic a

240 immune response pathways in addition to the TLR9 pathway, which is mainly activated by the CpG motif

241 Dectin-1 and TLR9 play distinct roles in the recognition and inductio

242 High-expression tlr9 polymorphisms have been linked to the development o

243 issue factor antibody or genetic deletion of TLR9 prevented these changes, whereas depleting monocyte

244 s activated by nucleic acid-sensing TLR7 and TLR9 proliferate and secrete immune globulins.

245 conclusion, we identified a pathway by which TLR9 promotes renal Treg accumulation in AKI.

246 somal toll-like receptors (TLR3, TLR7/8, and TLR9), proteins involved in innate immune signaling.

247 mulated cells activated the mTOR pathway via TLR9 receptor to induced MMP-7, beta-glucan-stimulated c

248 y binding to endosomal Toll-like receptor-9 (TLR9; refs 1-5).

249 ovide a new perspective on the complexity of TLR9 regulation by proteolytic cleavage and offer potent

250 mice showed increased responses to Tlr7 and Tlr9, respectively.

251 agments with resultant activation of TLR7 or TLR9, respectively.

252 ts suggest a mechanism by which TGF-beta and TLR9 responses in myofibroblasts collaborate to drive ra

253 sive monocytes capable of sustaining chronic TLR9 responses in vivo.

254 determine the mechanisms allowing sustained TLR9 responses to develop in vivo.

255 sis as a peripheral source of newly produced TLR9 responsive monocytes capable of sustaining chronic

256 Monocytes were identified as the main TLR9-responsive cell and accumulated in peripherally inf

257 lved in the RA-mediated production of IgG in TLR9/RP105-stimulated B cells.

258 We further demonstrate a novel role for TLR9 signal strength in central tolerance, providing ins

259 nsitivity to ANA is modulated by strength of TLR9 signal, because stronger TLR9(B6) signals, but not

260 TK is an essential axis integrating BCRs and TLR9 signaling in human B cells.

261 for IL-10 production downstream of TLR7 and TLR9 signaling in multiple immune cell types.

262 tudies identify a non-MyD88 pathway of TLR7/ TLR9 signaling in neurons and provide a mechanism for ho

263 Here, we examine the role for TLR9 signaling in response to A. baumannii infection.

264 TLR9 signaling is specifically essential in pDCs but not

265 s and report the first in vivo evidence that TLR9 signaling mediates the induction of periodontal bon

266 Understanding the regulation of the TLR9 signaling pathway and the involvement of A20 as a l

267 32) is also a dominant-negative regulator of TLR9 signaling.

268 riggered NETosis is independent of classical TLR9 signaling.

269 mice show that TLR2, -3, -4, and -7, but not TLR9, signaling can replace viral infection and augment

270 ated, TLR9-dependent signaling and deficient TLR9-specific CD11b up-regulation.

271 pDC did not restore ERK1/2 activation after TLR9 stimulation and only weakly affected IFN-beta and I

272 rapy, whereas clonal B cells unresponsive to TLR9 stimulation persist for at least 24 weeks, although

273 Chronic TLR9 stimulation resulted in stably differentiated alpha

274 After in vitro TLR9 stimulation, ERalpha deficiency significantly reduc

275 or (TACI), and CD23 activation markers after TLR9 stimulation.

276 ired phosphorylation of the MAPK ERK1/2 upon TLR9 stimulation.

277 M levels were elevated upon ex vivo anti-BCR/TLR9 stimulation.

278 ed lung fibroblasts to Toll-like receptor 9 (TLR9) stimulation by CpG-oligodeoxynucleotide (CpG-ODN)

279 significantly weaker to Id-3F7.A10 than did TLR9-sufficient mice, suggesting that the cognate BCR ef

280 type and a risk-enhancing association of the TLR9 TA haplotype with pustule formation; logistic regre

281 ist), suggesting possible cross talk between TLR9, TLR4, and TLR2.

282 inhibitors of endosomal Toll-like receptors (TLR9, TLR7) that activate MYD88.

283 Trafficking of TLR9 to A. fumigatus and C. albicans phagosomes requires

284 To determine whether an inability of TLR9 to detect endogenous DNA could explain the absence

285 nopeptidase IRAP, the trafficking of CpG and TLR9 to lysosomes and signaling via TLR9 were enhanced i

286 c redistribution and accumulation of cleaved TLR9 to phagosomes.

287 of NF-kappaB-->ZEB1 signaling represses the TLR9 (toll-like receptor 9), IFNG, MCP-1 (monocyte chemo

288 actor FHOD4, which slowed the trafficking of TLR9 toward lysosomes.

289 n tyrosine kinase activation is required for TLR9 trafficking to beta-1,3 glucan-, A. fumigatus-, and

290 tion of beta-1,3 glucan by Dectin-1 triggers TLR9 trafficking to beta-1,3 glucan-containing phagosome

291 less severe AKI than did reconstitution with Tlr9(-/-) Tregs.

292 first proof-of-concept evidence implicating TLR9-triggered inflammation in periodontal disease patho

293 yofibroblasts in vitro, but the mechanism of TLR9 up-regulation and progression of fibrosis are unkno

294 Thus, endosomal retention of TLR9 via the interaction of IRAP with the actin cytoskel

295 CpG and TLR9 to lysosomes and signaling via TLR9 were enhanced in DCs and in mice following bacteria

296 t not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were more susceptible to P. aeruginosa adhes

297 B cells express the innate receptor, TLR9, which signals in response to unmethylated CpG sequ

298 In contrast to TLR9, which suppressed activation of the FOXO3A pathway,

299 nd initiated signaling through both TLR7 and TLR9, which was not utilized in the absence of Ab.

300 Engaging TLR9 with CpG oligonucleotide contributes to the develop