ライフサイエンスコーパス: poly I

1 c fibroblasts (MEFs) challenged with EMCV or poly(I .

2 on in mice when administered with long-chain poly(I . C) [poly(I . C)LC] as an adjuvant.

3 , CpG, tripalmitoyl-Cys-Ser-Lys (Pam(3)CSK), poly(I . C), flagellin, and R848.

4 such as encephalomyocarditis virus (EMCV) or poly(I . C).

5 coli-derived CS proteins in combination with poly(I . C)LC induced potent multifunctional (interleuki

6 ata suggest that full-length CS proteins and poly(I . C)LC or GLA-SE offer a simple vaccine formulati

7 was significantly less potent than that with poly(I . C)LC.

8 en administered with long-chain poly(I . C) [poly(I . C)LC] as an adjuvant.

9 d to BALB/c mice following VACV infection or poly(I-C) inoculation, consistent with differences in in

10 arcoma cell line SW-1353 were activated with poly(I-C) of different molecular weights as a dsRNA mimi

11 increased 2-5A levels in response to IFN and poly(I-C), a double-stranded RNA mimic compared with the

12 cient mice were treated with TGFbeta, IL-13, poly(I-C), or TSLP by osmotic pump.

13 (PBMCs) were stimulated with TGFbeta, IL-13, poly(I-C), or TSLP.

14 of MMP13 messenger RNA (mRNA) expression by poly(I-C), regardless of its mode of delivery.

15 Poly(I-C)-treated mice showed high levels of cutaneous T

16 educed induction of MMP13 mRNA expression by poly(I-C).

17 Intranasal pretreatment of aged mice with poly(I.C) (a TLR3 agonist) and, to a lesser extent, CpG,

18 V infection as well as following exposure to poly(I.C) (a Toll-like receptor 3 [TLR3] stimulus) and 5

19 Treatment with poly(I.C) and flagellin but not with synthetic lipoprote

20 o identified a potential cellular target for poly(I.C) by showing that treatment inhibited virus repl

21 ditionally, NLRX-1 interacts with RV RNA and poly(I.C) in polarized airway epithelial cells.

22 Here, we demonstrate that both RV RNA and poly(I.C) interact with NLRX-1 (a newly discovered dsRNA

23 (LPS) of Toll-like receptor 4 (TLR4) and by poly(I.C) of TLR3 but not of TLR7/8 with imiquimod.

24 Poly(I.C) pretreatment upregulated beta interferon (IFN-

25 These results suggest that intranasal poly(I.C) should be evaluated as a prophylactic agent in

26 In addition, both RV and poly(I.C) stimulated mitochondrial ROS, the generation o

27 eta promoter after Sendai virus infection or poly(I.C) treatment.

28 protection [90% to 100% survival rate after poly(I.C) treatment] against lethal MA15 or IAV challeng

29 Poly(I.C), a double-stranded RNA (dsRNA) mimetic, also c

30 en following exposure to the synthetic dsRNA poly(I.C), a potent PKR agonist.

31 s able to block its induction by transfected poly(I.C), an analog of cytoplasmic double-stranded RNA

32 pitope, the Toll-like receptor (TLR) agonist poly(I.C), and a costimulatory anti-CD40 antibody.

33 idence that the two LR miRNAs cooperate with poly(I.C), interferon (IFN) regulatory factor 3 (IRF3),

34 trong IFN response to Sendai virus (SeV) and poly(I.C), NV RNA replicates efficiently and generates d

35 rto Rico/8/34 virus inactivated vaccine as a poly(I.C)- or a squalene-based adjuvant.

36 ide-activated splenic lymphocytes but not in poly(I.C)-activated splenic lymphocytes.

37 HEV replication in hepatoma cells inhibited poly(I.C)-induced beta interferon (IFN-beta) expression

38 ination is a key step in their activation in poly(I.C)-induced IFN induction.

39 the host innate immune response and rescued poly(I.C)-induced inhibition of VSV replication.

40 In infected HeLa cells, EV68 inhibits poly(I.C)-induced interferon regulatory factor 3 (IRF3)

41 In vivo, poly(I.C)-induced neutrophilia and mucosal chemokine pro

42 ls, the X domain (or macro domain) inhibited poly(I.C)-induced phosphorylation of interferon regulato

43 was used to find FWPV-encoded modulators of poly(I.C)-mediated ChIFN2 induction.

44 out mutant of FWPV still blocked transfected poly(I.C)-mediated induction of the beta IFN (ChIFN2) pr

45 We also demonstrated that RV or poly(I.C)-stimulated NADPH oxidase 1 (NOX-1) partially a

46 or experimental adjuvants alum, AddaVax, and poly(I.C).

47 tment of astrocytes or oligodendrocytes with poly(I.C).

48 us and Sendai virus and to transfection with poly(I.C).

49 fied 5'pppRNA structures, RIG-I aptamers, or poly(I.C).

50 us (RV) and polyinosinic-polycytidilic acid [poly(I.C)], a double-stranded RNA (dsRNA) mimetic, cause

51 ed dendritic cells (MoDCs) were treated with poly (I: C) of TLR3 ligand and imiquimod of TLR7 ligand,

52 tion antibody were significantly enhanced in poly (I: C), imiquimod along with inactivated PRRSV grou

53 The TLR3 agonist poly (I:C) activated TLR3 pathway and inhibited tumor ce

54 n barrier repair genes, that the TLR3 ligand Poly (I:C) also induced expression and function of tight

55 preparation of Saccharomyces cerevisiae, or poly (I:C) was coated on a microneedle with inactivated

56 ing and lipolysis attenuated by TNFalpha and Poly (I:C).

57 hallenged with Pam3Cys and LPS, but not with Poly (I:C).

58 Polyinosinic-polycytidylic acid [Poly (I:C)], a dsRNA receptor ligand, activates Rac via

59 of our study was to elucidate the effect of poly I:C (1, 10, or 100 mug/mouse) in a mouse model of B

60 pregnant mice treated with the TLR3 agonist poly I:C (P-PIC).

61 Here we show that Poly I:C (TLR3 agonist) or R848 (TLR7 agonist) do not ac

62 Poly I:C activation of nonhematopoietic cells was also i

63 rmal conditions remained diabetes-free after poly I:C administration.

64 ient mice and wild-type animals treated with poly I:C and an antibiotic developed disease.

65 Poly I:C and ISCOMs can alter Ag uptake and/or processin

66 Combining poly I:C and ISCOMs caused substantial death of dendriti

67 For CD4 T cells, combining poly I:C and ISCOMs increased the frequency of multifunc

68 illustrate how combining adjuvants, such as poly I:C and ISCOMs, that modulate Ag processing and hav

69 Both prenatal Poly I:C and postnatal LPS produced changes in locomotor

70 ating ovalbumin (OVA) as a model antigen and poly I:C as the adjuvant in an ionic complex.

71 deficient mice treated with antibiotics plus poly I:C had higher bacterial diversity compared with di

72 In conclusion, our data prove that poly I:C has potential anti-tumor activity in a mouse mo

73 Second, poly I:C induced activation of phagocyte NADPH oxidase i

74 growth factor FLT3L followed by intratumoral poly I:C injections expanded and activated CD103(+) DC p

75 First, Mac-1 facilitated poly I:C internalization through the activation of PI3K

76 The uptake of poly I:C into cells was reduced in the presence of ssDNA

77 l and physical response to the dsRNA mimetic poly I:C is dependent on signaling via MyD88 when it is

78 y airway cells with the synthetic RLR ligand poly I:C led to greater IFN induction at 37 degrees C re

79 11b subunit, interacted and colocalized with poly I:C on the surface of macrophages.

80 were sensitized to necroptosis triggered by poly I:C or interferons.

81 Poly I:C promoted uptake and retention of Ag, whereas IS

82 PKR activation in infected macrophages with poly I:C resulted in parasite death.

83 ental etiology, treatment of human CTBs with poly I:C significantly increased HIF-1alpha, NF-kappaBp5

84 rophils incubated with supernatants from the Poly I:C stimulation experiment.

85 int-blockade efficacy and combined FLT3L and poly I:C therapy can enhance tumor responses to checkpoi

86 inally, the administration of sulfatrim plus poly I:C to TLR9-deficient mice resulted in alterations

87 tly reduced the intensity of insulitis after poly I:C treatment.

88 nst metastatic lung cancer progression after poly I:C treatment.

89 The sensitizing effect of Poly I:C was specific for the TLR-3 pathway because mice

90 comparable response magnitude, but combining poly I:C with ISCOMs induced a high frequency of CD127(+

91 the efficacy of a therapeutic intervention (poly I:C) and a potential vaccine [Venezuelan equine enc

92 polyinosinic-polycytidylic acid sodium salt (poly I:C) to target Toll-like receptor 3 (TLR3) in endos

93 N) and polyribosinic-polyribocytidylic acid (Poly I:C) were uniquely able to enhance the T cell-primi

94 atment with polyinosinic:polycytidylic acid (poly I:C), a synthetic double-stranded RNA and agonist o

95 Poly inosinic:poly cytidylic acid (Poly I:C), a synthetic ligand for TLR-3, was administere

96 Polyinosinic-polycytidylic acid (poly I:C), a TLR3 ligand, is currently being tested in h

97 LR3 ligand, polyinosinic:polycytidylic acid (poly I:C), and immunostimulatory complexes (ISCOMs).

98 t mice with polyinosinic:polycytidylic acid (Poly I:C), which simulates a viral infection, on gestati

99 ral mimetic polyinosinic:polycytidylic acid (poly I:C).

100 TLR3 ligand polyinosine-polycytidylic acid (poly I:C).

101 sponse to sequential challenges with LPS and Poly I:C, a TLR3 ligand, which was physiologically assoc

102 data warrant further exploration of PGN and Poly I:C, alone or in combination, as DC-targeted adjuva

103 tion in vivo, we administered ssDNA-ODNs and poly I:C, alone or in combination, via the intranasal ro

104 When stimulated with Poly I:C, ATC/TTC haplotype, cells significantly up-regu

105 We show that toll-like receptor 3 agonist Poly I:C, combined with exogenous EC growth factors, tra

106 d macrophages with lipopolysaccharide (LPS), poly I:C, or zymosan.

107 macrophages that were activated by cytosolic poly I:C, reoviral RNA, or bacterial RNA.

108 ted GSK3beta ubiquitination is essential for poly I:C-dependent cytokine production by promoting the

109 cally associates with TRAF6 in a TLR3 ligand poly I:C-dependent manner.

110 rther supported the notion that the PGN- and Poly I:C-induced effects were mediated through binding t

111 The enhanced priming capacity of Poly I:C-stimulated DCs was associated with a strong upr

112 as arrested after a single administration of poly I:C.

113 elicited by polyinosinic:polycytidylic acid (poly I:C; a synthetic dsRNA) in mouse sera and livers, a

114 enatal immune challenge by the viral mimetic poly(I:C) (polyriboinosinic polyribocytidilic acid).

115 serine-lysine-4 (P3C; TLR1/2 ligand) but not poly(I:C) (TLR3 ligand) or LPS (TLR4 ligand) reverted th

116 ) mice amplified HA synthesis in response to poly(I:C) + TSG-6 in a manner similar to WT MASM cells,

117 Furthermore, poly(I:C) abrogated TGF-beta-induced fibrotic responses

118 In summary, in-poly(I:C) activates two distinct antitumor pathways in P

119 In response to poly(I:C) addition, the metastatic IECs also induced the

120 After poly(I:C) administration, a rapid reduction in parasite

121 ndependent trafficking, whereas signaling by poly(I:C) alone was not, suggesting that the LL-37-poly(

122 ling endosomes by a different mechanism than poly(I:C) alone.

123 s following stimulation with the TLR ligands Poly(I:C) and CpG.

124 Residues in LL-37 that contact poly(I:C) and facilitate oligomerization in vitro were m

125 that the genetic defect was the cause of the poly(I:C) and HSV-1 phenotypes.

126 Furthermore, Poly(I:C) and LPS induced endothelial to mesenchymal tra

127 Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response th

128 NF-kappaB responses to LUBAC, TNFalpha, and poly(I:C) and sensitizes cells to TNFalpha-induced cell

129 Therefore, we show that the increased in-poly(I:C) apoptotic efficacy is due to a higher binding

130 esponses to the double-stranded RNA analogue poly(I:C) are reduced in mouse macrophages.

131 y-disrupting inflammatory events mimicked by poly(I:C) are regulated by IL-10 and depend on the effec

132 vanted with polyinosinic:polycytidylic acid (poly(I:C) as an adjuvant (Vaccine-NP).

133 On the other hand, we show that in-poly(I:C) binding to cytosolic receptors MDA5 and RIG-I

134 These data show that H1N1 and poly(I:C) can induce alphavbeta6 integrin-dependent TGFb

135 LL-29 prevented LL-37 . poly(I:C) co-localization to endosomes containing TLR3.

136 :C) alone was not, suggesting that the LL-37-poly(I:C) complex trafficked to signaling endosomes by a

137 (I:C)) compared with the 12-fold higher free poly(I:C) concentration in PC3 and DU145 cells.

138 In contrast, poly(I:C) decreased (P < 0.05) ABCB1, TLR-3, and TLR-4 m

139 A poly(I:C) effect was also observed on MG TECs.

140 These poly(I:C) exosomes demonstrate enhanced trafficking to t

141 with 0.1 to 10 mug/mL LPS or 1 to 50 mug/mL poly(I:C) for 4 or 24 hours; mRNA levels, protein expres

142 his Vaccine-NP was compared to ovalbumin and poly(I:C) formulated in a similar manner (Control-NP) an

143 Surprisingly, the inhibitory effects of poly(I:C) in fibroblasts were independent of TLR3 and we

144 The presence of poly(I:C) increased the accumulation of LL-37 in Rab5 en

145 Vaccine formulations of peptide+CpG-ODN or Poly(I:C) induced selective production of proinflammator

146 onstrated that the synthetic analog of dsRNA poly(I:C) induces apoptosis in the androgen-dependent PC

147 e results suggest that the double hit of PGN+poly(I:C) induces preterm labor via reduction of a2V exp

148 In addition, poly(I:C) injections specifically increase thymic expres

149 In adult mice that received daily poly(I:C) injections, but not in offspring with prenatal

150 In C57Bl/6 mice, poly(I:C) instillation significantly increased accumulat

151 Our results indicate that poly(I:C) is a particularly favorable TLR agonist for DC

152 The synthetic double-stranded RNA poly(I:C) is commonly used as an adjuvant to boost CD8 T

153 tion of the RIG-I/MAVS pathway, such as when poly(I:C) is delivered intracellularly in a complex with

154 FN-beta stimulation by liposome-encapsulated poly(I:C) is markedly diminished in well-differentiated

155 Intracellular poly(I:C) markedly augments an inward voltage-sensitive

156 tude of the IL-8 response stimulated by pure poly(I:C) matched or even exceeded that of IFN-beta.

157 In this study, we investigated the effect of poly(I:C) on controlling enteric infection by the protoz

158 We analysed the in vitro effect of poly(I:C) on the release of IL-17A by spleen and lung CD

159 However, prior treatment of mice with poly(I:C) or mouse CMV infection resulted in increased L

160 n cells and organs but showed no response to poly(I:C) or R848.

161 agonists inhibited the IL-17A production by poly(I:C) plus alpha-GalCer in the same models.

162 Addition of the adjuvants CpG-ODN or Poly(I:C) preferentially amplified Teffs over Tregs, dra

163 Furthermore, we discovered that poly(I:C) pretreatment primes B-cells to the activation

164 ata herein demonstrate that the TLR3 agonist poly(I:C) promotes IFN-beta expression and R(+)WIN55,212

165 By using genetic inhibition of different poly(I:C) receptors, we demonstrate the crucial role of

166 Treatment of WT mice with poly(I:C) resulted in excessive trophoblast migration in

167 acrophage responses to lipoteichoic acid and poly(I:C) signaling via TLR2 and TLR3, respectively, was

168 with LPS, monophosphoryl lipid A (MPLA), or poly(I:C) significantly reduced plasma LPS-elicited proi

169 demonstrate that dsRNA signaling induced by poly(I:C) specifically triggers the overexpression of al

170 the first to show that exosomes derived from poly(I:C) stimulated cells induce in vivo macrophage M1-

171 well-differentiated), we observed that pure poly(I:C) stimulated IFN-beta mainly through the TLR3/TR

172 Previously, we have shown that poly(I:C) stimulates lung fibroblasts to accumulate an e

173 Poly(I:C) stimulation of lung fibroblasts isolated from

174 F-alpha was found to be in a level seen with poly(I:C) stimulation only, indicating that alpha7-nAChR

175 on-metastatic IECs, which did not respond to poly(I:C) stimulation.

176 Poly(I:C) strongly induced IFNa in cell lines, whereas t

177 g and that LL-37 can redirect trafficking of poly(I:C) to effect signaling by TLR3 in early endosomes

178 neonatal mice how gut flora synergizes with poly(I:C) to elicit protective intestinal immunity again

179 Mx1-Cre:ROSA mice, which were injected with poly(I:C) to label mature hepatocytes, were fed with the

180 developed nephritis following treatment with poly(I:C) to mimic microbial stimulation.

181 of our study was to identify conditions for poly(I:C) to selectively upregulate IFN-beta in airway e

182 olved in the remarkable apoptosis induced by poly(I:C) transfected by Lipofectamine (in-poly(I:C)) co

183 PGN+poly(I:C) treatment disturbed adherens junction proteins

184 In wild type (WT) mice, poly(I:C) treatment induced expansion of NKG2D(+) uNK ce

185 Upon poly(I:C) treatment, IFNAR-deficient mice displayed both

186 les under certain cellular stresses, such as poly(I:C) treatment.

187 LPS and poly(I:C) treatments increased (P < 0.01) IL-8 and chemo

188 We observed that poly(I:C) up-regulates transcription of UNC93B1 and prom

189 Poly(I:C) upregulated the in vitro IL-17A production by

190 be-associated molecular patterns pam3CSK4 or Poly(I:C) was not sufficient to block hyperactivity in a

191 gnaling by cells induced with both LL-37 and poly(I:C) was sensitive to inhibitors that affect clathr

192 When poly(I:C) was used to produce exosomes together with ova

193 lycan (PGN) and polyinosinic:cytidylic acid (poly(I:C)) (ligands for TLR4, TLR2 and TLR3, respectivel

194 tor ligands polyinosinic-polycytidylic acid (poly(I:C)) and flagellin.

195 etic analog polyinosinic:polycytidylic acid (poly(I:C)) bind and activate TLR3.

196 y poly(I:C) transfected by Lipofectamine (in-poly(I:C)) compared with the 12-fold higher free poly(I:

197 esponses to polyinosinic-polycytidylic acid (poly(I:C)) resulting from three independent N-ethyl-N-ni

198 NA analogue polyinosinic:polycytidylic acid (poly(I:C)) was dependent on TLR3 and UNC-93B in all cell

199 TLR3 ligand polyinosinic-polycytidylic acid (poly(I:C)), a dsRNA analog, caused dose- and time-depend

200 Polyinosine-polycytidylic acid (poly(I:C)), a Toll-like receptor 3 (TLR3) agonist used a

201 injection of artificial double-stranded RNA (poly(I:C)), we observed severe liver damage in type I IF

202 absence of polyinosinic-polycytidylic acid (poly(I:C)), which elicits RLR accumulation at mitochondr

203 ccharide or polyinosinic:polycytidylic acid (poly(I:C))-induced necroptosis and inflammatory signalli

204 hannel agonist or treatment with cytoplasmic poly(I:C), a mimic of viral dsRNA, activates this pathwa

205 NFkappaB2 is induced in response to poly(I:C), a mimic of viral dsRNA.

206 ere we mimicked viral immune activation with poly(I:C), a synthetic analog of double-stranded RNA, an

207 Poly(I:C), acting via TLR3, induces p52-dependent transa

208 were upregulated for LTA, LPS, Poly(dT), and Poly(I:C), and 12, 142, 249, and 16 genes were downregul

209 en TSG-6 was administered in the presence of poly(I:C), and TSG-6 did not exert any effect on its own

210 poly(I:C), but not flagellin, induced cell death and cas

211 a protein was released by cells treated with poly(I:C), but remained intracellular in cells treated w

212 In contrast, LPS, MPLA, and CpG-ODN, but not poly(I:C), improved the host response to a Pseudomonas a

213 retinal pigment epithelial cells with LPS or poly(I:C), indicating an increase in the glycolytic acti

214 higher FRET efficiencies in the presence of poly(I:C), indicating that RNA causes these proteins to

215 eptor (PRR) ligands, including lipid A, LPS, poly(I:C), poly(dA:dT), and cGAMP, induce cGAS expressio

216 Even in the absence of poly(I:C), polyclonally activated naive IRF3(-/-) CD8 T

217 re downregulated for LTA, LPS, Poly(dT), and Poly(I:C), respectively, with at least a 1-fold change r

218 lls had lower FRET signal in the presence of poly(I:C), suggesting that LGP2 oligomers disperse so th

219 ens and matured with either the TLR-3 ligand poly(I:C), the TLR-4 ligand LPS or the TLR-9 ligand CpG-

220 ntigen) and polyinosinic-polycytidylic acid (poly(I:C), viral antigen) would decrease P-gp and BCRP i

221 -induced CXCL10 was triggered by immobilized poly(I:C), was only modestly affected by inhibition of e

222 gens during exosome production together with poly(I:C), we obtained a Dexo vaccine capable of inducin

223 1 promoter region contains binding sites for poly(I:C)- and type I interferon-inducible regulatory el

224 n is a critical inflammatory mediator during poly(I:C)-induced acute lung injury and, in association

225 trate the crucial role of TLR3 and Src in in-poly(I:C)-induced apoptosis.

226 Furthermore, caspase-1 inhibition prevented poly(I:C)-induced caspase-3/7 activation.

227 transporter protein UNC93B1 was required for poly(I:C)-induced CXCL10 production.

228 ating receptor NKG2D play a critical role in poly(I:C)-induced fetal demise.

229 creased HA synthesis occurred during active, poly(I:C)-induced HA synthesis and did not occur when TS

230 and did not occur when TSG-6 was added after poly(I:C)-induced HA synthesis was complete.

231 RvD1 strongly suppressed the viral mimic poly(I:C)-induced IL-6 and IL-8 production and proinflam

232 We observed that poly(I:C)-induced IRF3 activation in CD8 T cells repress

233 L-1RA both rescued IFNAR-deficient mice from poly(I:C)-induced liver damage, directly linking the der

234 loid cells is essential to protect mice from poly(I:C)-induced liver damage.

235 sican in mediating inflammatory responses in poly(I:C)-induced lung inflammation using a tamoxifen-in

236 Collectively, these results indicate that poly(I:C)-induced molecular responses of macrophages cou

237 In vivo GSI treatment prevents PGN+poly(I:C)-induced preterm delivery by 55.5% and increase

238 ary, Notch signaling is activated during PGN+poly(I:C)-induced preterm labor, resulting in upregulati

239 ly reduced in uterus and placenta during PGN+poly(I:C)-induced preterm labor.

240 enta, uterus, and fetal membranes during PGN+poly(I:C)-induced preterm labor.

241 y elevated in uterus and placenta during PGN+poly(I:C)-induced preterm labor.

242 processing) significantly diminished the PGN+poly(I:C)-induced secretion of M1- and M2-associated cyt

243 B pathways, by inhibiting the formation of a poly(I:C)-induced signaling complex composed of TAK1, TA

244 nvolvement in influenza (A/PR/8/34 H1N1) and poly(I:C)-induced TGFbeta activation.

245 ance of our data was investigated in vivo in poly(I:C)-injected mice.

246 tingly, although the 14-3-3 proteins inhibit poly(I:C)-mediated RANTES production, 14-3-3 proteins au

247 Notably, CD8 T cells sensitized in poly(I:C)-pretreated mice failed to fully up-regulate IL

248 hages during virus or virus-like infections, poly(I:C)-stimulated macrophage-like RAW264.2 cells or m

249 Coincidentally, poly(I:C)-stimulated macrophages showed attenuated expre

250 However, when poly(I:C)-stimulated macrophages were challenged with ni

251 uated the release of IL-6 and TNF-alpha from poly(I:C)-stimulated macrophages.

252 sites, including Thr286 on CaMKIIalpha, from poly(I:C)-stimulated RAW264.7 cells, of which 28 are exp

253 attenuated intracellular Ca(2+) signal from poly(I:C)-stimulated RAW264.7 cells.

254 ked extracellular release of IL-36gamma from poly(I:C)-treated cells.

255 ynthase was significantly upregulated in PGN+poly(I:C)-treated placenta and uterus.

256 increased and polarization was skewed in PGN+poly(I:C)-treated uterus toward double-positive CD11c(+)

257 ctivation of caspase-1 were increased in PGN+poly(I:C)-treated uterus, which could induce pyroptosis.

258 Blockade of NKG2D in poly(I:C)-treated WT mice led to normal pregnancy outcom

259 Accordingly, in poly(I:C)-treated WT, but not IFNAR-deficient mice, mono

260 timulated, such as via liposomal delivery of poly(I:C).

261 ated by stimulation with TLR ligands LPS and poly(I:C).

262 ephalomyocarditis virus or transfection with poly(I:C).

263 93B1 is triggered through TLR3 activation by poly(I:C).

264 fected with Sendai virus or transfected with poly(I:C).

265 ponsible for TLR3 signaling induced by LL-37-poly(I:C).

266 binding to HA cables produced in response to poly(I:C).

267 ns such as the synthetic double-stranded RNA poly(I:C).

268 ired for Sp1 gene transcription activated by poly(I:C).

269 omplexes than those formed in the absence of poly(I:C).

270 TLR2 (Pam3Cys), TLR4 (LPS), and TLR3 agonist Poly(I:C).

271 hritis following exposure to the TLR3 ligand poly(I:C).

272 tion or in adulthood to the immune stimulant poly(I:C).

273 e same changes in TLR and RLR sensitivity as poly(I:C).

274 lycan (PGN) and polyinosinic:cytidylic acid (poly(I:C).

275 so seen in vivo after treatment of mice with poly(I:C).

276 ke receptor 4 (TLR4), but not TRIF-dependent poly(I:C)/TLR3.

277 gonist) and polyinosinic-polycytidylic acid [poly(I:C); a TLR3 agonist], modeling Gram-positive bacte

278 n; however, polyinosinic:polycytidylic acid [poly(I:C)] can also suppress autoimmune disease.

279 jected with polyinosinic:polycytidylic acid [poly(I:C)] during pregnancy as a model of prenatal immun

280 viral mimic polyinosinic-polycytidylic acid [poly(I:C)] in primary human lung epithelial cells.

281 Polyinosinic-polycytidylic acid [poly(I:C)] is a known inducer of IFN-beta but also costi

282 The TLR3 ligand [poly(I:C)] markedly suppressed VEGF secretion and stimul

283 activity of polyinosinic-polycytidylic acid [poly(I:C)] on IL-17A production by CD1d-activated iNKT c

284 ant polyriboinosinic-polyribocytidylic acid [poly(I:C)] on TRP metabolism in the placenta and its imp

285 lication of polyinosinic-polycytidylic acid [poly(I:C)] or LPS induces production of allergen-specifi

286 LR3 agonist polyinosinic:polycytidylic acid [poly(I:C)] to induce pro-caspase-11 expression were as s

287 d TLR ligand pairs [R-848 plus either LPS or Poly(I:C)] were superior to individual agents at boostin

288 hetic dsRNA polyinosinic-polycytidylic acid [poly(I:C)], a mimetic of viral RNA, rapidly reprograms m

289 mic polyriboinosinic-polyribocytidilic acid [Poly(I:C)], the bacterial endotoxin lipopolysaccharide,

290 icrovascular ECs (HDMECs) treated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists sh

291 h the dsRNA polyinosinic-polycytidylic acid [poly(I:C)], which induces IFNs via the viral RNA recepto

292 y(dT)], and polyinosinic-polycytidylic acid [Poly(I:C)].

293 ighly heterogeneous responses to IFNalpha or poly-I:C (a TLR3 ligand) when they were applied individu

294 are mostly limited to simple sequences like poly-I:C and poly-A:U.

295 ual to or substantially greater than that of poly-I:C depending on the delivery vehicle.

296 In contrast, a combination of IFNalpha and poly-I:C uniformly enhanced the production of CXCL10 and

297 tocytes after stimulation with extracellular poly-I:C, a TLR3 ligand.

298 kappaB activation in SKOV3 cells compared to poly-I:C, indicating that it is a powerful activator of

299 As polyinosinic-polycytidylic acid (poly[I:C]), which mimics double-stranded RNA (dsRNA), st

300 in adult Mx1-Cre Srsf2(flox/flox) mice upon poly(I):poly(C) injection demonstrated a significant dec