ライフサイエンスコーパス: type I interferon

1 iquitinase A (DUBA), a negative regulator of type I interferon.

2 ly, STING-dependent expression of anti-tumor type I interferon.

3 on of viral infections and the production of type I interferon.

4 op mutants were unable to block induction of type I interferon.

5 wever, ZIKV-induced CH25H was independent of type I interferon.

6 respond with rapid and massive production of type I interferon.

7 rferonopathies are thought to be mediated by type I interferon.

8 ondition where the other T/F strains induced type I interferon.

9 ts and ultimately leads to the production of type I interferons.

10 ated lactate interacts with MAVS to suppress type I interferons.

11 ated lactate interacts with MAVS to suppress type I interferons.

12 iviral signaling protein (MAVS) to stimulate type I interferons.

13 sease characterized by the overexpression of type I interferons.

14 inhibits the expression of genes induced by type I interferons.

15 odulate the immune response by production of type I interferons.

16 the nucleus and initiates the expression of type I interferons(21).

17 unogenic cell death and the local release of type I interferons across murine cancer cell lines.

18 Type I interferons act via a specific signaling pathway

19 in STIM1 strongly enhanced the expression of type I interferons after viral infection and prevented t

20 ed to cancer vaccine systems utilizing novel type I interferon agonists as immune adjuvants, radiatio

21 show in a mouse model of LCMV infection that type I interferon alters the expression and function of

22 This correlated with increased type I interferon and an IFN-related gene signature, and

23 tranasal IgG4/7 antibodies and lack of nasal type I interferon and chemokine induction.

24 P synthase (cGAS), leads to the synthesis of type I interferon and involves signaling through STING,

25 bits major pro-inflammatory pathways such as type I interferon and nuclear factor-kappaB signaling.

26 The role of type I interferon and PPRs in rhinovirus-induced asthma

27 We sought to compare bronchial mucosal type I interferon and PRR expression at baseline and aft

28 ng human MKs with DENV selectively increased type I interferons and IFITM3.

29 ogram is the production of cytokines such as type I interferons and IL-1beta.

30 f IFN genes (STING), leading to induction of type I interferons and inflammatory cytokines.

31 Multiple type I interferons and interferon-gamma (IFN-gamma) are

32 focused response that predominantly involves type I interferons and interferon-related genes, whereas

33 romoting the transcription of genes encoding type I interferons and other cytokines and mediators tha

34 , mediating the transcriptional induction of type I interferons and other genes that collectively est

35 gnaling cascade leading to the production of type I interferons and other immune mediators.

36 ngeal swabs demonstrated that in addition to type-I interferon and interleukin-6-dependent inflammato

37 s that contain DNA trigger the production of type-I interferons and inflammatory cytokines through cy

38 and the transcription factor IRF3 to induce type-I interferons and other cytokines(10,11).

39 nterferon regulatory factors (IRFs) 3 and 7, type I interferon, and interferon-stimulated genes.

40 Cytokines involved in humoral, type I interferon, and T-helper (Th) 17 responses were a

41 SNP at Toll-like receptor 3, which triggers type I interferon antiviral responses in mothers infecte

42 lpha to suppress EBV reactivation.IMPORTANCE Type I interferons are important for controlling virus i

43 smacytoid DCs (pDCs), the major producers of type I interferon, are principally recognized as key med

44 ugh pattern recognition receptors and induce type I interferons as well as proinflammatory cytokines

45 f PTEN, there was increased co-expression of type I interferon-associated genes with PTEN on single c

46 ol, preventing accumulation and a subsequent type I interferon-associated inflammatory response.

47 he inflammation mediated by the induction of type I interferons by STING.

48 had reduced ACE2 expression, indicating that type I interferon contributes mechanistically to this ef

49 We report here a mouse model in which type I interferon-deficient mice infected with a clinica

50 e mice are resistant to CCHFV infection, and type I interferon-deficient mice typically develop a rap

51 ceptor (IFNAR) knockout mice to evaluate the type I interferon dependence of the mutant Sting phenoty

52 Moreover, we show that type I interferons do not control SARS-CoV-2 replication

53 A role for itaconate in the regulation of type I interferons during viral infection has also been

54 our previous studies, we reported increased type I interferon expression and the upregulation of sev

55 f receptors for the IL-23/IL-12 pathways and type I interferon family, where it pairs with JAK2 or JA

56 Type I interferons have a crucial role in the progressio

57 We found that in monocytes, type I interferon (IFN) and cytokine responses to infect

58 macrophages induces elevated basal levels of type I interferon (IFN) and interferon stimulated genes

59 ly in infection, HIV-1 suppresses peripheral type I interferon (IFN) and interferon-stimulated gene (

60 t the ability of Lpro to block expression of type I interferon (IFN) and other IFN-stimulated genes.

61 depletion, mediated by CD8 T cell-intrinsic type I interferon (IFN) and signal transducer and activa

62 Type I interferon (IFN) antiviral responses and SARS-CoV

63 pneumonia, and we have shown previously that type I interferon (IFN) contributes to the pathogenesis

64 Type I interferon (IFN) drives pathology in systemic lup

65 Elevated levels of type I interferon (IFN) during pregnancy are associated

66 Mechanistically, type I interferon (IFN) expressed following infection pr

67 A relative to gRNA levels not only inhibited type I interferon (IFN) expression in infected cells thr

68 A type I interferon (IFN) gene signature distinguished DMA

69 on, TBK1-dependent IRF3 phosphorylation, and type I interferon (IFN) gene transcription downstream of

70 erferon regulatory factor 7 (IRF7)-dependent type I interferon (IFN) immunity to influenza virus in 6

71 Type I interferon (IFN) induced by virus infections duri

72 og, Oasl2, enhance RNA-sensor RIG-I-mediated type I interferon (IFN) induction and inhibit RNA virus

73 Type I interferon (IFN) is a key cytokine that curbs vir

74 Type I interferon (IFN) is a major output of STING signa

75 oyed by HSV-1 to downregulate the anti-viral type I interferon (IFN) mediated immune responses.

76 ia upregulation of several components of the type I interferon (IFN) pathway.

77 the B-cell receptor (BCR) with simultaneous type I interferon (IFN) produced by dendritic cells, esp

78 We found that melanoma TEV downregulated type I interferon (IFN) receptor and expression of IFN-i

79 Unlike TLR7-mediated disease, which requires type I interferon (IFN) receptor signaling, TLR9-driven

80 ession of genes involved in inflammation and type I interferon (IFN) response as a function of indivi

81 cts on virus infections and on the antiviral type I interferon (IFN) response have not been adequatel

82 The type I interferon (IFN) response is an ancient pathway t

83 Type I interferon (IFN) response is commonly recognized

84 individuals and is predicted by an elevated type I interferon (IFN) response(2-7).

85 tantial insight into how FMDV suppresses the type I interferon (IFN) response, but it is largely unkn

86 coid-inducible factor Tsc22d3, which blocked type I interferon (IFN) responses in dendritic cell (DC)

87 utation also increased early infectivity and type I interferon (IFN) responses in mouse bone marrow-d

88 nity, which include the evasion of antiviral type I interferon (IFN) responses.

89 Type I interferon (IFN) signaling engenders an antiviral

90 Activation of type I interferon (IFN) signaling was detected in both r

91 onuclear cells from the patients, downstream type I interferon (IFN) signaling was transcriptionally

92 crophages and epithelial cells had increased type I interferon (IFN) signaling, potentially through u

93 6 regulated a gene repertoire reminiscent of type I interferon (IFN) signalling, including upregulati

94 l for breast cancer stimulates intratumoural type I interferon (IFN) signalling, which enhances the a

95 ty to harm the endothelium, and responses to type I interferon (IFN) stimulation are evident among LD

96 l encephalitis in the Western world, and the type I interferon (IFN) system is important for antivira

97 e classical role of IRF-7 as a stimulator of type I interferon (IFN) transcription, there were no glo

98 of MG53 in macrophages leads to increases in type I interferon (IFN) upon infection.

99 disease activity, SLE-associated antibodies, type I interferon (IFN), and complement C3, correlated w

100 signatures characterized by higher levels of type I interferon (IFN), expansion and expansion/surviva

101 eficient cells secreted increased amounts of type I interferon (IFN), which could be limited by CGAS

102 ulated following IAV infection in AM through type I interferon (IFN)-dependent signaling.

103 SG15, stabilize USP18, a potent inhibitor of type I interferon (IFN)-I.

104 -2, Vaccinia virus, and Zika virus through a type I interferon (IFN)-independent mechanism.

105 Here, we report that type I interferon (IFN)-inducible miR-128 directly targe

106 ultiple strategies to confront or evade host type I interferon (IFN)-mediated antiviral responses in

107 se, characterised by increased expression of type I interferon (IFN)-regulated genes and a striking s

108 Type I interferon (IFN)-response signatures in tubular c

109 omputational modeling to investigate how the type I interferon (IFN)-responsive regulatory network op

110 roptosis by mammalian reovirus requires both type I interferon (IFN)-signaling and viral replication

111 line of defence leading to the production of type I interferon (IFN).

112 robial stimuli and mediates the induction of type I interferon (IFN).

113 lls (pDCs) and blunts systemic production of type I interferon (IFN).

114 We show that activation of the type I interferon (IFN)/IFNalpha receptor (IFNAR) axis a

115 HSV-1 actively suppresses production of type I interferon (IFN); our data reveal that IL-36 over

116 mulating plasmacytoid dendritic cells-(pDCs)-Type I interferon (IFN-I) and acts as autoantigen for pa

117 Plasmacytoid dendritic cells (pDCs) produce type I interferon (IFN-I) and are traditionally defined

118 Type I interferon (IFN-I) and T helper 17 (TH17) drive p

119 onogenic disorders characterized by enhanced type I interferon (IFN-I) cytokine activity.

120 Uncontrolled expression of type I interferon (IFN-I) drives autoimmunity, necessita

121 tive CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct

122 lexes are present in vivo and correlate with type I interferon (IFN-I) in SSc blood, and that CXCL4-p

123 As for other bacteria, PRR-stimulated type I interferon (IFN-I) induction has been proposed as

124 Type I interferon (IFN-I) is crucial for promoting antiv

125 tory stimuli by inhibiting the NF-kappaB and type I interferon (IFN-I) pathways.

126 osphorylation of IRF3 (not TBK1) and enhance type I interferon (IFN-I) production in macrophages.

127 Type I interferon (IFN-I) provides effective antiviral i

128 LRC3 is a negative regulator that attenuates type I interferon (IFN-I) response by sequestering and a

129 S1/2 in establishing local replication and a type I interferon (IFN-I) response in the colon.

130 rred early after infection, correlating with type I interferon (IFN-I) responses.

131 In this report, we evaluate type I interferon (IFN-I) sensitivity of SARS-CoV-2 rela

132 Type I interferon (IFN-I) signaling and IFN-I-producing

133 that Toll-like receptor 7 (TLR7) sensing and type I interferon (IFN-I) signaling in B-1 cells contrib

134 ate immune pathways, including the antiviral type I interferon (IFN-I) system.

135 of genes involved in expansion and survival, type I interferon (IFN-I), and JAK/STAT pathways.

136 inst infections mainly through production of type I interferon (IFN-I).

137 aimed to identify novel viral regulators of type I interferon (IFN-I).

138 ression depends on Mtb-induced production of type I interferon (IFN-I).

139 dendritic cells (pDCs) are a major source of type I interferon (IFN-I).

140 ivate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I).

141 initiating capacity through activation of a type I interferon (IFN-I)/STAT1 pathway when caspases ar

142 Type I interferons (IFN) are being rediscovered as poten

143 Type I interferons (IFN) mediate antiviral effects throu

144 og phase of viral growth, while secretion of type I interferons (IFN) occurred with delayed kinetics.

145 Notably, the production of type I interferons (IFN-alpha/beta), IFN-stimulated gene

146 Type I interferons (IFN-I) are a major antiviral defense

147 The concept that type I interferons (IFN-I) are essential to antiviral im

148 Type I interferons (IFN-I) are key innate immune effecto

149 ch activates AHR, limiting the production of type I interferons (IFN-I) involved in antiviral immunit

150 lammasomes(1-6) and are often insensitive to type I interferons (IFN-I), but are restricted by IFN-ga

151 ells neither induce nor respond to canonical type I interferons (IFN-I).

152 various cytokines and chemokines, including type I interferons (IFN-I).

153 duces robust production of type III, but not type I, interferon (IFN).

154 transcriptionally derepressed and activate a type-I interferon (IFN-I) response.

155 esponses, characterized by the production of type-I interferons (IFN) including IFNbeta.

156 of innate immune signaling (RIG-I, MDA5, or type I interferon [IFN] signaling) or infection with WNV

157 on downregulation of the IFNAR1 chain of the type I interferon (IFN1) receptor.

158 Type I interferons (IFNalpha and IFNbeta) directly regul

159 Type I interferons (IFNalpha/beta) are critical mediator

160 ls detect a viral infection, they initiate a type I interferon (IFNs) response as part of their innat

161 Type I interferons (IFNs) (IFN-alpha, IFN-beta) and type

162 respond to intracellular dsRNA by expressing type I interferons (IFNs) and inducing apoptosis, but th

163 Increased levels of type I interferons (IFNs) and nucleosome-associated doub

164 infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines

165 Type I interferons (IFNs) are essential mediators of ant

166 During HIV-1 infection, type I interferons (IFNs) are induced, and their effecto

167 Type I interferons (IFNs) are key mediators of the innat

168 Type I interferons (IFNs) can reprogram the cholesterol

169 DNA damage and type I interferons (IFNs) contribute to inflammatory res

170 reciated; ii) neutralizing autoantibodies to type I interferons (IFNs) could provide protection again

171 Type I interferons (IFNs) induce expression of multiple

172 neutrophil-mediated inflammation.IMPORTANCE Type I interferons (IFNs) possess a range of biological

173 Type I interferons (IFNs), including alpha IFN (IFN-alph

174 ation is characterized by elevated levels of type I interferons (IFNs), which can block HIV-1 replica

175 of which is the expression of genes encoding type I interferons (IFNs).

176 tionally repressing STAT1/2 and secretion of Type I Interferons (IFNs).

177 ion factor with many target genes, including type I interferons (IFNs).

178 G is phosphorylated, leading to induction of type I interferons (IFNs).

179 es to produce RNAs that lead to induction of type I interferons (IFNs).

180 innate antiviral immune response mediated by type I interferons (IFNs).

181 (2020) convincingly demonstrate that type I interferons (IFNs-I) promote dysregulation of iro

182 st decades, studies have widened the role of type-I interferons (IFNs) in disease, from antivirus def

183 the levels of inflammatory mediators such as type I interferons, IL-6, TNF-alpha or IL-1beta in respo

184 ging phenotype accompanying inborn errors of type I interferon immunity.

185 lation of antiviral effectors in response to type I interferons.IMPORTANCE Viral infection triggers t

186 eronopathies) characterized by expression of type I interferon in the brain.

187 Basal levels of type I interferon in the long-term infected bat cells we

188 nd PLP2 mutant viruses trigger production of type I interferon in vitro and are attenuated in mice, f

189 tor superfamily of transcription factors, by type I interferons in response to inflammatory signals.

190 into endogenous and exogenous activation of type I interferons in the tumour and its microenvironmen

191 del of STING hyperactivation and the role of type I interferons in this system.

192 The designed CHIKV variants became potent type I interferon inducers and acquired a less cytopathi

193 Loss of this type-I-interferon-inducible protein, which we refer to a

194 ctural protein (NSs) has been shown to block type I interferon induction(7-11) and facilitate disease

195 NA-sensing cGAS-cGAMP-STING pathway mediates type I interferon inflammatory responses in immune cells

196 Treatment of EBV-infected cells with type I interferon inhibits reactivation of the virus, wh

197 Type I interferon is essential for promoting an antivira

198 Interferon-alpha (IFNalpha), a type I interferon, is expressed in the islets of type 1

199 ic acids is the primary mechanism by which a type I interferon-mediated antiviral response is trigger

200 ea shortly after influenza infection through type I interferon-mediated production of the chemokine C

201 Here we show that type I interferons, one of the first mediators produced

202 Type I interferons, particularly interferon-alpha (IFN-a

203 HMGB1) release activates the host TLR4/MyD88/type I interferon pathway and Batf3 dendritic cell-depen

204 clusters, including 101 CpGs in genes in the Type I Interferon pathway, and we validate these associa

205 ding kinase 1/interferon regulatory factor 3 type I interferon pathway.

206 sensor of cytoplasmic DNA that activates the type-I interferon pathway(2).

207 he porcine HB (pHB) is mediated by promoting type I interferon pathways.

208 Type I Interferon-primed ISG15-knockout porcine and rhes

209 , an anti-viral cytosolic receptor activated type I interferon production, and NLR (nucleotide-bindin

210 leading to activation of inflammatory genes, type I interferon production, autophagy, and cell death.

211 er-inducing interferon-beta (TRIF)-dependent type I interferon production, inhibition of tumor necros

212 have been thought to contribute to excessive type I interferon production.

213 DNA release, and DNA sensor-STING-dependent type I interferon production.

214 recognition and for subsequent activation of type I interferon production.

215 rts antiviral activity through regulation of type I interferon production.

216 ern recognition receptors (PRRs), leading to type I interferon production.

217 nducible gene I (RIG-I), thereby stimulating type I interferon production.

218 ease of cGAMP stimulates STING signaling and type I interferons production in APCs, resulting in the

219 to define the roles of cGAS, IRF3, IRF7, the type I interferon receptor (IFN-alpha and IFN-beta recep

220 onditional deletion of STING, or blockade of type I interferon receptor I restored the immunoinhibito

221 s of Janus-associated kinase 1 (JAK1) to the type I interferon receptor.

222 and administrated using different routes in type-I interferon receptor deficient A129 mice.

223 rference includes suppression of hundreds of type I interferon-regulated genes due to lower interfero

224 Cancer Cell, Ortiz and colleagues show that type I interferon regulates extracellular vesicle uptake

225 plicative capacity (p = 0.0005) and are more type I interferon-resistant (p = 0.007) than those trans

226 active human TB disease, with dominance of a type I interferon response and neutrophil activation and

227 , results in a virus that activates both the type I interferon response and the type III interferon r

228 further demonstrated that ROS suppressed the type I interferon response by oxidizing Cysteine 147 on

229 tion or defective negative regulation of the type I interferon response can lead to autoinflammation.

230 g and nonexpressing mice, but enrichment for type I interferon response gene changes was specifically

231 might protect virus-infected cells from the type I interferon response in cells undergoing lytic vir

232 at the DUB mutant virus activated an earlier type I interferon response in macrophages and exhibited

233 xed with nucleic acids triggers an antiviral type I interferon response in neuroglia, resulting in co

234 mammalian target of rapamycin signaling, and type I interferon response pathways, particularly follow

235 signaling adaptor that is essential for the type I interferon response to DNA pathogens.

236 hat IDV induced mild inflammation and that a type I interferon response was not necessary in IDV clea

237 te sensing of incoming virus and the ensuing type I interferon response within B-1 cells are responsi

238 /-) mice show marked early activation of the type I interferon response, and C9orf72(-/-) myeloid cel

239 ll lines provoked an entirely cGAS-dependent type I interferon response, including IRF3 phosphorylati

240 ing DNMTi and HDAC6i results in an amplified type I interferon response, leading to increased cytokin

241 protein levels, and consequently a dampened type I interferon response, which compromised the abilit

242 poptotic cells within tumors and triggered a type I interferon response.

243 potentially involved in regulating the host type I interferon response.

244 by encoding viral proteins that inhibit the type I interferon response.

245 w avidity and remain cytoplasmic trigger the type I interferon response.

246 racy, rather than uniquely to antagonize the type I interferon response.

247 nfections through a mechanism independent of type I interferon response.

248 SV-1DeltaUL41N) resulted in a cGAS-dependent type I interferon response.

249 te and adaptive immune cells and a prominent type-I interferon response.

250 ly discovered in a bat, suppresses antiviral type I interferon responses in both human and bat cells.

251 s, and blocking STING suppresses hyperactive type I interferon responses in C9orf72(-/-) immune cells

252 monocyte-derived DCs activated antiviral and type I interferon responses, molecules associated with i

253 n of host responses, including inhibition of type I interferon responses, suppression of dendritic ce

254 the cyclic dinucleotide cGAMP, resulting in type I interferon responses.

255 nsplantable BC, largely reflecting increased type I interferon secretion by malignant cells and direc

256 the cellular innate response, especially via type I interferon secretion, and perform efficient viral

257 ct both viral replication and IAV-associated type I interferon secretion.

258 cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming

259 n STING N153S mice develops independently of type I interferon signaling and cGAS.

260 n in vitro and subsequently drives increased type I interferon signaling and cytotoxic T-cell activat

261 erstanding of how ionizing radiation induces type I interferon signaling and how to amplify this sign

262 USP18 down-regulates type I interferon signaling by blocking the access of Ja

263 ative contributions of these two pathways in type I interferon signaling depend on cell type and/or g

264 the concurrent activation and inhibition of type I interferon signaling during infection.

265 dent RNA-sensing pathway are responsible for type I interferon signaling induced by ionizing radiatio

266 anti-tumor phenotype; this process required type I interferon signaling irrespective of adaptive imm

267 ssembly, including molecules involved in the type I interferon signaling pathway and caspase-6.

268 2 tegument protein binds to a protein in the type I interferon signaling pathway Tyk2 and inhibits th

269 ically interacted with genes enriched in the type I interferon signaling pathway, apoptosis, or TP53

270 ition, an enrichment in the IL-12 family and type I interferon signaling pathways was observed among

271 activation of innate immune recognition and type I interferon signaling pathways, but downregulation

272 nd is punctuated by a late prenatal spike in type I interferon signaling that promotes perinatal HPC

273 t the DNMTi 5-Azacytidine (5AZA-C) activates type I interferon signaling to increase IFNgamma(+) T ce

274 the involvement of two distinct pathways in type I interferon signaling upon DNA damage.

275 fetal head was observed in a small subset of type I interferon signaling-deficient immunocompromised

276 ta were used to study the functional role of type-I interferon signaling in ACE2 expression.

277 s in BRISC that disrupt SHMT2 binding impair type I interferon signalling in response to inflammatory

278 in conjunction with a global suppression of type I interferon-signalling pathway and an aberrant exp

279 atients with C9-ALS/FTD all show an elevated type I interferon signature compared with samples from p

280 AT1 in myeloid cells increases expression of type I interferon stimulated genes in response to LPS.

281 ation promotes the upregulation of antiviral type I interferon-stimulated genes (ISGs), we hypothesiz

282 interferon genes (STING; N153S) upregulates type I interferon-stimulated genes and causes perivascul

283 uired for the proper shutdown of a subset of type I interferon-stimulated genes as inflammation subsi

284 Type I interferon, T cells, and, most importantly, signa

285 ination with radiation by assessing TBK1 and Type I interferon (T1IFN) signaling as well as tumor gro

286 sis of HIV-1 negative vaccinees reveals that type I interferons that activate the IRF7 antiviral prog

287 While hundreds of genes are induced by type I interferons, their roles in restricting the influ

288 MP)(9-12), which stimulates the induction of type I interferons through the STING-TBK1-IRF-3 signalli

289 lic GMP-AMP, which mediates the induction of type I interferons through the STING-TBK1-IRF3 signallin

290 ctivation ex vivo triggered psoriasiform and type I interferon tissue responses in NLP psoriasis.

291 ic CRISPR screen in cells prestimulated with type I interferon to identify antiviral genes that restr

292 pression of EBV BGLF2 reduces the ability of type I interferon to inhibit virus reactivation.

293 ells was not due to compensation by enhanced type I interferon transcripts to thus inhibit virus prod

294 tivation of STING and enhanced expression of type I interferons under resting conditions in mice and

295 ich is sensed to stimulate the production of type I interferons via the stimulator of interferon gene

296 ion status was defined by QFT, enrichment of type I interferon was observed.

297 on RNAs that induced increased expression of type I interferon, which was dependent on the cytoplasmi

298 nflammatory cytokines, but the production of type I interferons, which are key antiviral mediators, i

299 CE Viral infection triggers the secretion of type I interferons, which in turn induce the expression

300 otice" the infection and respond by inducing type I interferons, which limits virus replication.