ライフサイエンスコーパス: interferon

1 unction of additional cytokines (such as the interferons).

2 s intrinsic, as stem cells are refractory to interferon.

3 e disease, leading to aberrant activation of interferon.

4 exaggerated responsiveness to type I and II interferons.

5 ility of ruxolitinib and renewed interest in interferons.

6 fficacy and safety of recombinant adenovirus interferon alfa with Syn3 (rAd-IFNalpha/Syn3), a replica

7 INTERPRETATION: Pegylated interferon alfa-2a can induce durable haematological and

8 afety and efficacy of REP 2139 and pegylated interferon alfa-2a in patients with chronic HBV and hepa

9 Pegylated interferon alfa-2a induced haematological (66 [80%] of 8

10 ERPRETATION: Combined REP 2139 and pegylated interferon alfa-2a therapy is safe, well tolerated, and

11 into hepatoma cells and inhibit signaling by interferon alpha (IFNalpha), but have no effect on HCV-R

12 We record increased interferon alpha protein levels using digital ELISA, enh

13 rmal and stimulated conditions using chicken interferon-alpha (chIFN-alpha) and the attenuated infect

14 e studied the antiviral potency of pegylated interferon-alpha (pegIFNalpha) against HEV infections in

15 either treatment naive to or relapsed after interferon-alpha based therapy.

16 erentially mobilized by plerixafor with high interferon-alpha producing ability.

17 depression in the context of treatment with interferon-alpha, a widely used model to mimic depressio

18 activation (patients with HCV-infection and interferon-alpha, patients with major depression, and he

19 ng the IFN-alphas and IFN-beta, activate the interferon-alpha/beta receptor (IFNAR) complex.

20 polyethylene glycolyated (PEGylated) type-I interferon-alpha2b reduces the expression of many cytoki

21 ligonucleotides, while particles with strong interferon and mild pro-inflammatory cytokine induction

22 induces the subsequent expression of type I interferon and other proinflammatory cytokines.

23 onsecutively recruited before treatment with interferon and ribavirin for 24 to 48 weeks, according t

24 Treatment with interferon and ribavirin upregulated beta-defensin-1, bu

25 s been replaced by sofosbuvir plus pegylated interferon and ribavirin, and all-oral therapies where a

26 activity, even if some patients treated with interferon and ruxolitinib showed reduction of mutated a

27 Individual baboons expressed more gamma interferon and tumor necrosis factor alpha in response t

28 is in turn stimulates production of type III interferons and hence enhances tumour antigen presentati

29 not only through the induction of antiviral interferons and pro-inflammatory cytokines, but also by

30 ings reveal that signaling crosstalk between interferons and TNF is integrated at the level of chroma

31 ific gene expression was widely disturbed in interferon- and IRF8-regulated transcripts.

32 s, characterized by the upregulation of both interferon- and tumor necrosis factor-positive CD4(+) T

33 RVFV virulence depends on the interferon antagonist non-structural protein (NSs), whic

34 o process the viral polyprotein or act as an interferon antagonist, which involves deubiquitinating a

35 le proinflammatory gene ontologies, with the interferon-associated gene ontology exhibiting the highe

36 venting accumulation and a subsequent type I interferon-associated inflammatory response.

37 he outcomes depending on the strength of the interferon-based anti-viral response, consistent with th

38 Interferon-based regimens are associated with a substant

39 oinfection is similar to historic rates with interferon-based treatment, but with shorter treatment d

40 tes of sustained virologic response (SVR) to interferon-based treatments for chronic hepatitis C viru

41 1 (NS1) of WNV antagonizes the induction of interferon beta (IFN-beta) by interacting with and degra

42 ne (0DeltaNLS) is sensitive to inhibition by interferon beta (IFN-beta) in vitro and functions as a h

43 stant to ConA-induced liver damage, and anti-interferon beta antibody mitigated ConA/HSC-induced inju

44 lemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting mul

45 nce (TIR) domain-containing adapter-inducing interferon beta) and activation of the transcription fac

46 proinflammatory cytokines interleukin 1beta, interferon beta, and RANTES (regulated on activation of

47 nscriptional induction of interleukin 1beta, interferon beta, and RANTES in ZIKV-infected podocytes a

48 to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 yea

49 ose of 600 mg every 24 weeks or subcutaneous interferon beta-1a at a dose of 44 mug three times weekl

50 crelizumab and in 0.2% of those treated with interferon beta-1a.

51 crelizumab and in 2.9% of those treated with interferon beta-1a.

52 linical trial comparing early versus delayed interferon beta-1b treatment in 465 patients with a CIS.

53 PK3), TIR-domain-containing adapter-inducing interferon-beta (TRIF) and Z-DNA-binding protein 1 (ZBP1

54 Cytosolic DNA stimulates secretion of interferon-beta by cancer cells following activation of

55 res cyclic GMP-AMP synthase (cGAS)-dependent interferon-beta production and gasdermin D-dependent int

56 n ConA-induced liver injury directly via the interferon-beta/IRF1 axis, and by modulating properties

57 ro-inflammatory cytokines and high levels of interferons can be used as scaffolds to carry therapeuti

58 se of ribavirin causing hemolytic anemia and interferon causing cytopenias.

59 cirrhotic hepatitis C patients treated with interferon-containing regimens, it would have been expec

60 e refer to as IRAV, is induced by DENV in an interferon-dependent manner, displays antiviral activity

61 ort a model wherein the production of type I interferons driven by an autoimmune risk variant and tri

62 Interferon effector functions and autophagy are evolutio

63 s from rDEN2Delta30 and used them in a gamma interferon enzyme-linked immunosorbent spot assay to int

64 nscription factor DMRTA1 (27%) and antiviral interferon epsilon (IFNE, 19%).

65 We validated type-I interferon expression in neurofibroma by protein profili

66 The sofosbuvir-containing regimens without interferon for treatment of acute HCV in HIV-1 infected

67 investigated the effectiveness and safety of interferon-free DAA regimens in patients with advanced l

68 availability of, and national criteria for, interferon-free DAA reimbursement among countries in the

69 BACKGROUND & AIMS: Interferon-free direct-acting antiviral (DAA) therapies

70 owever, the ideal duration of treatment with interferon-free regimens, particularly in HIV-coinfected

71 associated cirrhosis and CSPH who had SVR to interferon-free therapy at 6 Liver Units in Spain.

72 NO after stimulation with recombinant badger interferon gamma (bdIFNgamma) or a combination of bdIFNg

73 ment of NKp44 triggered NK cell secretion of interferon gamma (IFN)-gamma and tumor necrosis factor a

74 ile analysis by RNA sequencing of subsets of interferon gamma (IFNG)-producing and non-producing cell

75 enotypic profile, as reflected by heightened interferon gamma and interleukin 17 (IL-17) production a

76 Production of interferon gamma by MAIT cells was dependent on monocyte

77 pment of colitis and increased expression of interferon gamma in the small intestine compared to wild

78 f HIV-1 Gag-specific CD8+ T cells expressing interferon gamma increased from baseline (0.09%) through

79 Furthermore, neonatal and interferon gamma knockout mouse models of C. parvum infe

80 Infection decreased interleukin 2 and interferon gamma production as well as the expression of

81 is issue, Overacre-Delgoffe et al. show that interferon gamma production by a subset of regulatory T

82 reserved HSPC-NK killing, proliferation, and interferon gamma production capacity, whereas AZA dimini

83 Biallelic null mutations in genes encoding interferon gamma receptor 1 or 2 (IFNGR1 or IFNGR2) resu

84 CCL17, CXCL8, CXCL10; and interleukin 2 and interferon gamma than children who survived, and lower l

85 (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor necrosis factor alpha, and granu

86 rized, and polyfunctional (ie, they produced interferon gamma, tumor necrosis factor alpha, granulocy

87 hted locus is a 100-kb region containing the interferon gamma-inducible protein 16 (IFI16) and absent

88 s increased the number of tumor-infiltrating interferon gamma-producing natural killer (NK) cells.

89 ldren and trends in tuberculin skin test and interferon gamma-release assays.

90 ied participants by quantitative QFT result (interferon-gamma <0.35 IU/mL, 0.35-4.00 IU/mL, and >4.00

91 was needed to prevent premature induction of interferon-gamma (IFN-gamma) expression in T cells and t

92 Mutations in genes affecting interferon-gamma (IFN-gamma) immunity have contributed t

93 onstrate that Ct growth inhibition occurs by interferon-gamma (IFN-gamma)-mediated depletion of intra

94 s, as well as low production of the cytokine interferon-gamma (IFN-gamma).

95 ed bystander naive CD8(+) T cells to produce interferon-gamma (IFNgamma) and granzyme B (GZB) in the

96 T cells to tumour rejection is unclear, but interferon-gamma (IFNgamma) is critical in most of the a

97 rentially secrete the Th1 and Th17 cytokines interferon-gamma and interleukin 17A, and are unresponsi

98 n during homeostasis and rapid production of interferon-gamma by NK cells after challenge.

99 ted to CMV-IE1 and CMV-pp65 were measured by interferon-gamma Elispot assay.

100 In addition, CD4 T cells produced less interferon-gamma in response to T-cell stimulation.

101 n have key roles in antigen presentation and interferon-gamma signalling, and correlate with cytolyti

102 T) was conducted by measuring granulysin and interferon-gamma to confirm the causalities.

103 cytotoxic granule constituents and produced interferon-gamma upon Fc-receptor engagement but not fol

104 ; p<0.0001), and compared with children with interferon-gamma values between 0.35-4.00 IU/mL (IRR 11.

105 However, QFT conversion at interferon-gamma values higher than 4.00 IU/mL was assoc

106 sion was common, following QFT conversion at interferon-gamma values up to 10 times the recommended t

107 -alpha and, to a lesser extent, IL-1beta and interferon-gamma were the most potent cytokines produced

108 s in the brain, including interleukin-1beta, interferon-gamma, and fractalkine as well as a decreased

109 ated decrease in tumor necrosis factor-beta, interferon-gamma, and monocyte chemoattractant protein-1

110 d proliferation of T cells and expression of interferon-gamma, tumor necrosis factor, and EOMES.

111 Moreover, angiotensin II infusion instigated interferon-gamma, which induced the expression of IDO an

112 The proinflammatory cytokine interferon-gamma-induced protein 10 (IP-10/CXCL10) was a

113 immune activation associated with increased interferon-gamma-inducible protein 10, interleukin (IL)-

114 Mtb-containing phagosomes and identified an interferon-gamma-stimulated and Rab20-dependent membrane

115 2 (CCR2), which was enhanced by exposure to interferon-gamma.

116 Stimulator of interferon genes (STING) was initially described as a se

117 Patients with stimulator of interferon genes (STING)-associated vasculopathy with on

118 loss of pattern recognition by stimulator of interferon genes (STING)-cGAS impaired interferon signal

119 late the NF-kappaB pathway and stimulator of interferon genes (STING)-dependent cytokine secretion.

120 Stimulator of interferon genes (STING, also known as MITA, MPYS, or ER

121 iptase activity suppressed the expression of interferon genes in uhrf1 mutants.

122 lic GMP-AMP synthase linked to stimulator of interferon genes) pathway, leading both to short-term in

123 n contrast to re-induction of HLA class-I by interferons, HDAC inhibitors did not interfere with the

124 10.6 months (95% CI, 8.5 to 14.4 months) for interferon (HR, 0.90; 95% CI, 0.72 to 1.12; P = .33).

125 AT1 phosphorylation in response to exogenous interferon (IFN) administration can be inhibited by rota

126 virus (HCV)-coinfected patients treated with interferon (IFN) and ribavirin (RBV), between 2000 and 2

127 pandemic H1N1 (pH1N1) virus was an effective interferon (IFN) antagonist but could not inhibit genera

128 the cyclic dinucleotide sensor stimulator of interferon (IFN) genes (STING) is critical for IFN and i

129 MP-AMP synthase (cGAS) and the stimulator of interferon (IFN) genes (STING), two crucial host factors

130 ized mouse model and demonstrate that type I interferon (IFN) is induced early during HIV infection a

131 The interferon (IFN) lambda 3/4 (IFNL3/4) locus, influencing

132 DKO HSPCs revealed the activation of p53 and interferon (IFN) pathways, which enforced cell cycling i

133 Both genes play significant roles in type I interferon (IFN) production and signalling.

134 the brain parenchyma has a functional type I interferon (IFN) response that can limit VSV spread at b

135 Type I interferon (IFN) signaling engenders an antiviral state

136 Consequently, MDA5-triggered type I interferon (IFN) signaling in the retinoic acid-inducibl

137 yopherin alpha (KPNA) proteins blocks type I interferon (IFN) signaling, which is a central component

138 utes to disease pathogenesis, with prominent interferon (IFN) signatures identified in both periphera

139 s a subset of genes previously classified as interferon (IFN) stimulated genes (ISGs) but that expres

140 acts as a selective repressor of the type I interferon (IFN) transcriptional program in response to

141 Interferon (IFN)-alpha treated chimpanzees and hepatitis

142 8 pooled lupus patient samples treated with interferon (IFN)-beta and perform eQTL analysis on 23 po

143 Effect of recombinant human interferon (IFN)-gamma or epithelial-derived IFN-gamma i

144 cells, and is characterized by production of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alph

145 uced Nos2 and Il1b mRNA levels and decreased interferon (IFN)-gamma, tumor necrosis factor (TNF)-alph

146 observe that EMT silences protective mucosal interferon (IFN)-I and III production associated with en

147 with hosts is greatly affected by the viral interferon (IFN)-inhibiting domains (IID).

148 al analysis approach, we identified a robust interferon (IFN)-stimulated gene response within microgl

149 However, the function of the HCMV-induced interferon (IFN)-stimulated genes (ISGs) in infected mon

150 tion of IRF3 and subsequent up-regulation of interferon (IFN)-stimulated genes (ISGs) in patients wit

151 ia cytoplasmic RNA sensors to produce type I interferon (IFN).

152 d primary microglia demonstrated the role of interferon (IFN)gamma and interleukin (IL)-4 in polarizi

153 gly, BST-2 upregulation in response to alpha interferon (IFN-alpha) was shown to increase the suscept

154 We screened the gamma interferon (IFN-gamma) and interleukin-10 (IL-10) respon

155 f interleukin-17A (IL-17A), IL-22, and gamma interferon (IFN-gamma) as well as the antimicrobial pept

156 In the livers of C57BL/6 mice, gamma interferon (IFN-gamma) controls intracellular Leishmania

157 ivo, wild-type mice were injected with gamma interferon (IFN-gamma) DNA or colony-stimulating factor

158 nt, while decreased mitogen-stimulated gamma interferon (IFN-gamma) production suggested immunomodula

159 In this study, we report that gamma interferon (IFN-gamma) treatment, but not IFN-alpha, -be

160 also observed increased production of gamma interferon (IFN-gamma), IL-5, IL-9, IL-17, and IL-22 and

161 as the production of TLR8-dependent type II interferon (IFN-gamma), TNF-alpha, and IL-12 in myeloid

162 hi(GFPuv)-infected BALB/c mice elicits gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF

163 onstrated that antigen-specific CD8(+) gamma interferon (IFN-gamma)-positive T-cell responses are ess

164 Furthermore, gamma interferon (IFN-gamma)-stimulated primary peritoneal neu

165 11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link be

166 rovar Typhimurium exploits the host's type I interferon (IFN-I) response to induce receptor-interacti

167 Furthermore, VA1 was sensitive to the type I interferon (IFN-I) response, as VA1 RNA levels were redu

168 roviral therapy (cART), low levels of type I interferon (IFN-I) signaling persist in some individuals

169 Lambda interferon (IFN-lambda) has potent antiviral effects aga

170 Era of listing was divided into interferon (IFN; 2003-2010), protease inhibitor (PI; 201

171 proinflammatory cytokines, including type I interferons (IFN).

172 Type I interferons (IFN-1) are cytokines that affect the expres

173 Pretreatment with type I interferons (IFN-alpha and IFN-kappa) increased IL-6 pro

174 toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid dendritic

175 Type I interferons (IFN-I) are critical in antimicrobial and an

176 iving force in immune exhaustion, and type I interferons (IFN-I) are emerging as critical components

177 Type I interferons (IFN-Is) can now be considered as the wedge

178 Type III interferons (IFN-lambdas) signal through a heterodimeric

179 kin 2 [IL-2], IL-4, IL-10, IL-17A, and gamma interferon [IFN-gamma]) and rendered T cells refractory

180 ch act as deubiquitinating and deISGylating (interferon [IFN]-stimulated gene 15 [ISG15]-removing) en

181 Type I interferons (IFNalpha/beta) are critical mediators of an

182 s the adaptor protein STING to induce type I interferons (IFNs) and other immune modulatory molecules

183 The type I interferons (IFNs) are a family of cytokines with divers

184 Interferons (IFNs) are essential components of the host

185 Type I interferons (IFNs) are essential mediators of antiviral

186 While induction of antiviral type I interferons (IFNs) is the major outcome of STING activat

187 Type I interferons (IFNs) play a central role in the immune def

188 ding strong induction of type I and type III interferons (IFNs).

189 ors show that the chronic presence of type I interferon in aged mouse brain impedes cognitive ability

190 thies) characterized by expression of type I interferon in the brain.

191 U-STAT2 might enhance the efficacy of type I interferons in many different clinical settings.

192 targeted against hepatitis C (ribavirin and interferon) in addition to immunosuppressive medical and

193 pharmacological approaches, we found that an interferon-independent mechanism involving Toll-IL-1-rec

194 the proinflammatory cytokines TNF and type I interferons induced transcriptional cascades that altere

195 iptomic studies revealed the presence of the interferon-induced antiviral myxovirus resistance (Mx) p

196 Interferon-induced transmembrane protein 3 (IFITM3) is a

197 d Arf1 activation, which led to formation of interferon-inducible GTPase-containing aggregates and ha

198 ining aggregates and hampered recruitment of interferon-inducible GTPases to vacuolar pathogens.

199 ll-autonomous immunity in metazoans predates interferon-inducible immunity and comprises primordial i

200 Moreover, interferon-inducible protein with tetratricopeptide repe

201 tetratricopeptide repeats 1, cystatin 1, and interferon-inducible protein with tetratricopeptide repe

202 in bat and human cells and the role of viral interferon-inhibiting domains in the host innate immune

203 ynthesis and increased sensitivity to type-1-interferon inhibition.

204 Genetic variation in the IFNL3-IFNL4 (interferon-lambda3-interferon-lambda4) region is associa

205 ation in the IFNL3-IFNL4 (interferon-lambda3-interferon-lambda4) region is associated with hepatic in

206 reduced hyperresponsiveness to type I and II interferons, normalized TH1 and follicular T helper cell

207 No difference in interferon or ISG expression was observed according to c

208 of 75 in the best available therapy group), interferon or pegylated interferon (ten [13%] of 75), pi

209 Treatment-experienced (prior interferon or pegylated interferon +/- ribavirin or sofo

210 tion or had received previous treatment with interferon or pegylated interferon, ribavirin, sofosbuvi

211 We identify the type 1 interferon pathway as a molecular mechanism by which c-M

212 The STING/type I interferon pathway enhances suppressive inflammation in

213 es suggest the involvement of TH1 and type 2 interferon pathways.

214 e, showed significant suppression of TEs and interferon pathways.

215 ciated with treatment responses to pegylated interferon (PEG-IFN)-based therapy in patients with chro

216 Pegylated interferon plus ribavirin has been replaced by sofosbuvi

217 first MVA-CMDR boost, vaccine-induced gamma interferon-positive (IFN-gamma(+)) Gag-specific T-cell r

218 The cell fate decision between interferon-producing plasmacytoid DC (pDC) and antigen-p

219 es in coordinating both virus-induced type I interferon production and apoptosis; however, the regula

220 Cytosolic nucleic acid sensing elicits interferon production for primary antiviral defense thro

221 nthetic analogue of histamine reduces type I interferon production in a mouse model of influenza infe

222 e it was evident in murine cells lacking the interferon receptor (IFNAR).

223 europathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-) ) mice,

224 fl) C57BL/6 (H-2(b)) mice lacking the type I interferon receptor in a subset of myeloid cells.

225 57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice against lethal ZIKV c

226 , consistent with overexpression of the four interferon receptors encoded on chromosome 21, and propo

227 on of a large subset of other IRF2-dependent interferon-regulated genes.

228 The second system is driven by interferon-regulated GTPases that promote rupture of pat

229 The transcription factor interferon regulatory factor (IRF)-5 is an important mod

230 The transcription factor interferon regulatory factor 1 (IRF-1) has a demonstrate

231 Interferon regulatory factor 1 (IRF-1) is a tumor suppre

232 actors nuclear factor kappaB (NF-kappaB) and interferon regulatory factor 3 (IRF-3), classically indu

233 y and confirmed that these miRNAs potentiate interferon regulatory factor 3 (IRF3) phosphorylation an

234 rom the site of inoculation independently of interferon regulatory factor 3 (IRF3)-, IRF7-, and IFNAR

235 microbial products, the transcription factor interferon regulatory factor 4 (IRF4) promotes regulator

236 Here, we demonstrated that interferon regulatory factor 4 (IRF4) was a key transcri

237 tion was found to be driven by 2 variants of interferon regulatory factor 4-dependent dermal type 2 c

238 Mutations and common polymorphisms in interferon regulatory factor 6 ( IRF6) are associated wi

239 Interferon Regulatory Factor 6 (IRF6) and TWIST1 are tra

240 Lastly translocation of interferon regulatory factor 7(IRF7) from the cytosol to

241 crosis factor-alpha, the chemokine CCL2, and interferon regulatory factor-5 (IRF5), a marker of infla

242 miR93 inhibits interferon regulatory factor-9 to decrease IRG1-itaconic

243 ed that IRG1 is not an miR93 target but that interferon regulatory factor-9, which can regulate IRG1

244 were conducted to examine the role of miR93-interferon regulatory factor-9-immunoresponsive gene-1 (

245 a-sensitive/resistant viruses indicates that interferon resistance maps to the env gene.

246 viral gene B19R, an inhibitor of the type I interferon response (NYVAC-C-KC-DeltaB19R).

247 ed impaired viral clearance, a slower type I interferon response and delayed production of virus-neut

248 R-neutralizing antibody after MI ablated the interferon response and improved left ventricular dysfun

249 Additionally, we found that the type I interferon response and sex hormones can alter both vira

250 We recently identified an activated interferon response associated with T21 in human cells o

251 G2D ligands after virus infection depends on interferon response factors activated by the detection o

252 stigated in A549 NPro cells where the type 1 interferon response had been attenuated.

253 cleosides, exogenous interferon stimulation, interferon response stimulation and HBV therapeutic vacc

254 Reduced CpG content dampened the interferon response to infection, promoting higher repli

255 These findings suggest that an exaggerated interferon response to viral infection by airway epithel

256 tokine-mediated gene activation, suppress an interferon response, and influence the transition into t

257 One such pathway, the type I interferon response, recognizes viral or mitochondrial D

258 25, although not all virus strains block the interferon response, suggesting alternative mechanisms f

259 irus B19 protein, an inhibitor of the type I interferon response.

260 hat activates RIG-I to promote the antiviral interferon response.

261 h induction of a microbiota-dependent type I interferon response.

262 st responses, including inhibition of type I interferon responses, suppression of dendritic cell matu

263 tion with anti-CD3/CD28 antibodies or type I interferon resulted in upregulation of distinct subsets

264 t-experienced (prior interferon or pegylated interferon +/- ribavirin or sofosbuvir plus ribavirin +/

265 vious treatment with interferon or pegylated interferon, ribavirin, sofosbuvir, or a combination of t

266 ssM produced high-titer IgG and robust gamma interferon-secreting T cell responses against the protei

267 ily and highlight the plasticity of type III interferon signaling and its therapeutic potential.

268 protein levels using digital ELISA, enhanced interferon signaling by RNA-Seq analysis and constitutiv

269 educed T-cell receptor, B-cell receptor, and interferon signaling in B cells.

270 ata suggest that this is not due to enhanced interferon signaling or an inhibition of clathrin-mediat

271 ional importance in the regulation of type I interferon signaling.

272 Functional analysis highlighted the roles of interferon signalling and the NFkappaB cascade, and we s

273 Here, we show that interferon signalling-competent SJL mice support chronic

274 e (CQ) extends the lifespan of ZIKV-infected interferon signalling-deficient AG129 mice.

275 or of interferon genes (STING)-cGAS impaired interferon signalling.

276 junction with a global suppression of type I interferon-signalling pathway and an aberrant expression

277 On the basis of the identification of an interferon signature in patients with CVID with secondar

278 odies (including anti-DNA IgG), and a type I interferon signature.

279 in humanized mice and modelled intrahepatic interferon stimulated gene (ISG) responses.

280 The signature's genes are: Interferon Stimulated Gene 15 (ISG15), Interleukin 16 (I

281 ntrols STAT1-mediated gene transcription via interferon stimulated response elements.

282 Viperin (RSAD2) is an interferon-stimulated antiviral protein that belongs to

283 ciency, decreased IFN-beta, IFN-lambda1, and interferon-stimulated chemokine gene expression.

284 UL46-expressing cell lines did not activate interferon-stimulated gene (ISG) transcription following

285 Although IFN-I signal via the interferon-stimulated gene factor 3 (ISGF3) complex cons

286 ugated with either ubiquitin (Ub) or Ub-like interferon-stimulated gene product 15 (ISG15).

287 Consistently, transcription of interferon-stimulated genes (eg, OAS1, ISG15, Mx1; each

288 n effects of each virus on the expression of interferon-stimulated genes were also investigated in A5

289 tiviral response measured by upregulation of interferon-stimulated genes, such as CXCL10 and DAI.

290 HD1 protein up-regulation upon type I and II interferon stimulation in primary human monocytes.

291 nhibitors, anti-sense nucleosides, exogenous interferon stimulation, interferon response stimulation

292 ally target crucial components of the type I interferon system.

293 Type 1 interferons (T1-IFN) are known to be a constituent of th

294 able therapy group), interferon or pegylated interferon (ten [13%] of 75), pipobroman (five [7%] of 7

295 CV treatment before or after inclusion (with interferon then with direct antiviral agents) and underw

296 t nucleos(t)ide analogue (NUC) and pegylated interferon therapies effectively help slow disease progr

297 n or sofosbuvir plus ribavirin +/- pegylated interferon therapy) patients without cirrhosis were rand

298 Interferon treatment increased rather than decreased HCV

299 priming depend not only on TLR9, but also on interferon type I signaling, and both mechanisms can be

300 creased the sensitivity of T cells to type I interferons, which interfered with effector T cell funct