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

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

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

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

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

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

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

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

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

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

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

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

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

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

17 studies using biotin-labeled viral dsRNA or poly(I.C) and cell lysate-derived or in vitro translated

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

19 d upon Toll-like receptor 3 stimulation with poly(I.C) double-stranded RNA or infection with herpes s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 1 in microglia activation to protect against poly (I:C) imparted neuropathology and altered behavior

49 activation in hematopoietic cells induced by poly (I:C) injection, all Mx1-CreCbfb+/56M mice develope

50 cells did not re-appear until 96 hours post poly (I:C) injury.

51 e acinar and progenitor cells, 24 hours post poly (I:C) introduction.

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

53 l in which polyinosinic: polycytidylic acid (poly (I:C)) was injected into pregnant mice.

54 ed (ds) RNA polyinosinic-polycytidylic acid (poly (I:C)) widely, but transiently, depleted the acinar

55 SMG recovery from the transient, but severe poly (I:C)-mediated injury and cellular depletion.

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

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

58 HPDLSCs were stimulated with Poly I:C (0.0001-1 ug/mL), Pam3CSK4 (1 ug/mL), and their

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

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

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

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

63 ors induced by simultaneous stimulation with Poly I:C and Pam3CSK4 were significantly higher compared

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

65 cent plasma, and of two antiviral therapies (poly I:C and remdesivir).

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

67 ytosis of H. influenzae was also impaired by poly I:C but not IFN-beta or IFN-gamma in COPD MDM.

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

69 The MDA5/LGP2 agonist high molecular weight poly I:C improved the antitumor effect of IR.

70 The toll-like receptor 3 agonist poly I:C increased expression of the mitochondrial citra

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

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

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

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

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

76 11b subunit, interacted and colocalized with poly I:C on the surface of macrophages.

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

78 CP-1, and OPG was significantly increased by Poly I:C or Pam3CSK4 to a similar extent.

79 f cells with exogenously-added type I IFN or poly I:C prior to infection limited the cytopathic effec

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

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

82 Addition of poly I:C significantly enhanced the expression and secre

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

89 n simultaneous stimulation with Pam3CSK4 and Poly I:C were significantly lower compared with Pam3CSK4

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

91 fection 5), polyinosinic:polycytidylic acid (poly I:C) 30 mug/ml, IFN-beta 10 mug/ml, IFN-gamma 10 mu

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

93 RNA mimic, Poly Inosinic-polycytidylic acid (Poly I:C) indicating defective dsRNA receptor signaling.

94 t mice with polyinosinic:polycytidylic acid (Poly I:C) on gestational day 12.5 to produce maternal im

95 R-3 agonist polyinosinic:polycytidylic acid (Poly I:C) on the expression of inflammatory markers and

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

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

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

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

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

101 and polyriboinosinic:polyribocytidylic acid (Poly I:C), RNA polymerase III (Pol lII)-dependent transc

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

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

104 PDL cells were treated with various doses of poly I:C, a TLR3 activator.

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

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

107 n and protein levels of OPG were enhanced by Poly I:C, but by lesser extent than by Pam3CSK4.

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

109 H. influenzae was significantly impaired by poly I:C, IFN-beta, and IFN-gamma in COPD cells.

110 rance for microbial stimuli, such as LPS and Poly I:C, resulting in increased production of key proin

111 In co-culture experiments, poly I:C-activated hPDL cells inhibited PBMCs proliferat

112 ipheral blood mononuclear cells (PBMCs) with poly I:C-activated hPDL cells was performed.

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

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

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

116 Knockdown of TLR3 using siRNA decreased the poly I:C-induced expression of these three molecules.

117 uto-phagosome and lysosome fusion, inhibited poly I:C-induced IDO and HLA-G expression, whereas cyclo

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

119 se together with cAMP-mediated inhibition of Poly I:C-stimulated IFNbeta expression.

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

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

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

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

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

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

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

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

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

129 In addition, Poly(I:C) also reduced right ventricular failure in esta

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

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

132 xposure of PBECs to concomitant TLR3 agonist poly(I:C) and HDM resulted in a significant reduction in

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

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

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

136 PRRs) TLR3 and RIG-I specifically respond to poly(I:C) and SeV respectively, subsequently triggering

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

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

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

140 adiotherapy, and linkage of the TLR3 agonist poly(I:C) as a model immune-oncologic agent.

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

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

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

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

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

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

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

148 tified: (a) in human infant AECs exposed to (poly(I:C) dsRNA) under different experimental conditions

149 odels via injection of a nonpathogenic agent poly(I:C) during pregnancy.

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

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

152 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

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

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

155 overexpressed, enhances endosomal escape of poly(I:C) in vitro.

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

157 Poly(I:C) increased TLR3 expression via IL-10 in rat end

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

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

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

161 to cause breakthrough alloimmunization, with poly(I:C) inducing alloimmunization even in the absence

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

163 MIA induced by poly(I:C) injections to P2rx7 WT mouse dams elicited an

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

165 (fl/fl) (mTORC1), either in all tissues upon poly(I:C) inoculation, or specifically in haemopoietic s

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

167 levels of IRF3 and TBK1 when challenged with poly(I:C) intracellularly.

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

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

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

171 Recipient treatment with poly(I:C) led to breakthrough anti-KEL alloimmunization

172 I IFNs with the double-stranded RNA mimetic poly(I:C) likewise produces pain hypersensitivity that i

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

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

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

176 reating cells with varying concentrations of poly(I:C) or arsenite to induce the ISR, we provide addi

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

178 Poly(I:C) or type I IFN administration was sufficient to

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

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

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

182 In vivo, high-dose Poly(I:C) reduced pulmonary hypertension in both rat mod

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

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

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

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

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

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

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

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

191 Upon poly(I:C) stimulation or viral infection, circRNAs are g

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 s, such as antigen (ovalbumin) and adjuvant (Poly(I:C)).

216 we report that TRAF3IP3 suppresses cytosolic poly(I:C), 5'ppp-dsRNA, and vesicular stomatitis virus (

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

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

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

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

221 rtment, interacts with the long dsRNA analog poly(I:C), and, when overexpressed, enhances endosomal e

222 epithelial cells (PBECs) in response to RSV, poly(I:C), house dust mite (HDM) or IL-33 using RT-qPCR,

223 ise apoptosis triggered by the dsRNA-homolog poly(I:C), however the exact mechanism by which this is

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

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

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

227 mice by administration of the viral mimetic, poly(I:C), on gestation day 12.

228 hallenge of HeLa cells with the dsRNA-analog poly(I:C), PGAM5 oligomers and high levels of PGAM5 were

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

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

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

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

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

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

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

236 1 promoter region contains binding sites for poly(I:C)- and type I interferon-inducible regulatory el

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

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

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

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

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

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

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

244 ow exacerbated HSC activation under systemic poly(I:C)-induced inflammation.

245 Our in vitro experiments showed that the poly(I:C)-induced innate production of IFN lambda in hum

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 -beta expression induced by Sendai virus and poly(I:C).

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

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

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

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

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

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

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

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

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

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

277 93B1 is triggered through TLR3 activation by poly(I:C).

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

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

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

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

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

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

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

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

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

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

288 Administration of synthetic [poly(I:C)] or genetic (Alu) dsRNA induces human osteobla

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

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

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

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

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

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

297 we compared the effects of MIA (injection of poly[I:C] to dam at gestational day 12.5), HI at postnat

298 absence of polyinosinic-polycytidilic acid (poly[I:C]), followed by the transfusion of murine red bl

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

300 LR3 agonist polyinosinic/polycytidylic acid (Poly[I:C]).

301 PolY is catalytically poor for subsequent extension from

302 ination with polyinosinic-polycytidylic acid-poly-I-lysine carboxymethylcellulose (poly-ICLC) every 3

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