ライフサイエンスコーパス: type I interferon

1 ppressed using antiviral regimens containing type I interferon.

2 FRs were enhanced by IL-12 but suppressed by type I interferon.

3 roteins (ISGylation) are strongly induced by type I interferon.

4 e upregulated, which were possibly driven by Type I Interferon.

5 nduction was demonstrated to be dependent on type I interferon.

6 xpression of viral response genes, including type I interferon.

7 L-2, stromal cell-derived factor 1alpha, and type I interferon.

8 ownstream of cGAMP synthase (cGAS) to induce type I interferon.

9 tes was primarily and transiently induced by type I interferon.

10 pus autoantigen Ro60, Alu retroelements, and type I interferon.

11 heral blood cells demonstrated activation of type I interferon.

12 us-1 infection due to enhanced production of type I interferon.

13 ned basal and ligand-triggered production of type I interferons.

14 (cGAMP) binds and activates STING to induce type I interferons.

15 In vitro, the viruses coped similarly with type I interferons.

16 ficiency resulted in increased production of type I interferons.

17 including the contribution of resistance to type I interferons.

18 1 to bind RIG-I and induce the expression of type I interferons.

19 nfectious pathogens by driving production of type I interferons.

20 ynthesis of host proteins, including that of type I interferon, a key component of the antiviral resp

21 g contributes substantially to production of type I interferons, a hallmark of pDC activation.

22 l activation of the IFN response through the type I interferon alpha/beta receptor (IFNAR).

23 ce with polyethylene glycolyated (PEGylated) type-I interferon-alpha2b reduces the expression of many

24 state that can be both distinct from that of type I interferon and can potently inhibit HIV-1 in prim

25 lf-nucleic acid species that trigger chronic type I interferon and inflammatory responses, leading to

26 mydial infection highlighted the role of the type I interferon and interleukin 10-mediated responses.

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

28 a concerted innate immune response involving type I interferon and pro-inflammatory cytokines to enab

29 cts herpes simplex virus (HSV) by activating type I interferon and proinflammatory responses upon sen

30 estrogens were able to control production of type I interferon and therefore play dual roles during i

31 n cytokine sensing, including in response to type I interferons and IL-3.

32 olygyrus infection upregulated expression of type I interferons and interferon-stimulated genes in bo

33 of TRIM29 enhanced macrophage production of type I interferons and protected mice from infection wit

34 n of alveolar macrophages, the expression of type I interferons and the production of proinflammatory

35 eceptors (RLRs, TLRs, PKR), or the cytokines type I interferons and TNF-alpha.

36 as initially thought, SUN2 is not induced by type I interferon, and that SUN2 silencing does not modu

37 Setdb2 expression depended on signaling via type I interferons, and Setdb2 repressed expression of t

38 for antigen signaling and antibodies against type I interferon are in the pipeline.

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

40 26-DNA complexes triggered the production of type I interferon by plasmacytoid dendritic cells via ac

41 acid-sensing Toll-like receptors (TLRs), and type I interferon can affect B-cell survival and decreas

42 Considering the fact that type I interferon decreases the activity of the choleste

43 ied to be key effector molecules in the host type I interferon defense system.

44 NA sensor cGAS and its adaptor STING induced type I interferon-dependent expression of IRF1, which dr

45 This case further implicates type I interferon-dependent innate immune activation in

46 achineries and key factors, inflammasome and type I interferon, directing cardinal innate immunity re

47 Type I interferons directly and negatively regulated mou

48 ta support a model wherein the production of type I interferons driven by an autoimmune risk variant

49 ed for a tumor marker.Significance: Targeted type I interferon elicits powerful antitumor efficacy, s

50 racterized as a transcriptional regulator of type I interferon expression after virus infection.

51 cleavage abrogated its capacity to activate type I interferon expression and limit replication of EV

52 metabolite desaminotyrosine (DAT) increases type I interferon expression, resulting in an improved i

53 protein plays a critical role in suppressing type I interferon expression.

54 tinoic acid-inducible gene 1 (RIG-I)-induced type I interferon expression.

55 We validated type-I interferon expression in neurofibroma by protein

56 inhibits MAVS protein-mediated apoptosis and type I interferon gene expression in a negative-feedback

57 Type I interferons have been shown to play a major role

58 Type I interferons have diametric roles in the host defe

59 Frequency of CD38, CD40 and type I interferon high responders was significantly incr

60 be particularly sensitive to the effects of type I interferon; however, little is known about the me

61 Neuronal antiviral responses are driven by type I interferon (IFN) and are crucial to controlling H

62 innate immune antiviral response, including type I interferon (IFN) and IFN receptor-mediated signal

63 Here, we show that type I interferon (IFN) and IRF-1 cooperate to control a

64 The host innate immune response mediated by type I interferon (IFN) and the resulting up-regulation

65 tibodies against nucleic acids and excessive type I interferon (IFN) are hallmarks of human systemic

66 The requirement of type I interferon (IFN) for natural killer (NK) cell act

67 Induction of type I interferon (IFN) in response to microbial pathoge

68 We sought to understand the role of type I interferon (IFN) in the innate and adaptive immun

69 ntly, we demonstrated that components of the type I interferon (IFN) induction pathway, particularly

70 Type I interferon (IFN) is critical for controlling path

71 Type I interferon (IFN) is crucial in host antiviral def

72 Type I interferon (IFN) is important for control of herp

73 a humanized mouse model and demonstrate that type I interferon (IFN) is induced early during HIV infe

74 Many viruses trigger the type I interferon (IFN) pathway upon infection, resultin

75 se (cGAS) in the DC cytosol, contributing to type I interferon (IFN) production and antitumor adaptiv

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

77 4SS-dependent cytokine responses, and robust type I interferon (IFN) production, and these pathways w

78 s chronic immune activation concomitant with type I interferon (IFN) production.

79 Parainfluenza viruses are known to inhibit type I interferon (IFN) production; however, there is a

80 Furthermore, mice lacking the type I interferon (IFN) receptor (IFNAR) became viremic

81 Here, we investigated the dynamics of the type I interferon (IFN) receptor, IFNAR1, and its effect

82 tosolic detection of nucleic acids elicits a type I interferon (IFN) response and plays a critical ro

83 major virulence factor known to suppress the type I interferon (IFN) response by inhibiting host cell

84 La involvement in regulating the type I interferon (IFN) response is controversial - acti

85 d that the brain parenchyma has a functional type I interferon (IFN) response that can limit VSV spre

86 We found that ALRs are dispensable for the type I interferon (IFN) response to transfected DNA liga

87 Innate immunity, via the type I interferon (IFN) response, plays an important rol

88 o the infected host cytosol induces a robust type I interferon (IFN) response.

89 urveillance pathway (CSP) is known to elicit type I interferon (IFN) responses, which are crucial to

90 her of upregulation of tumor-cell-autonomous type I interferon (IFN) signaling and a strong inflammat

91 Here, we discovered that a combination of type I interferon (IFN) signaling and interferon regulat

92 an essential DNA virus sensor that triggers type I interferon (IFN) signaling by producing cGAMP to

93 Type I interferon (IFN) signaling engenders an antiviral

94 as identified Toll-like receptors (TLRs) and type I interferon (IFN) signaling in both ischemia/reper

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

96 Recent findings indicate that antiviral type I interferon (IFN) signaling is induced by these tr

97 We previously found that host type I interferon (IFN) signaling is induced during Y. p

98 st responds to virus infection by activating type I interferon (IFN) signaling leading to expression

99 TBK1 is a component of the type I interferon (IFN) signaling pathway, yet the mecha

100 uggested a possible link between the Wnt and type I interferon (IFN) signaling pathways.

101 Using isotope tracer analysis, we show that type I interferon (IFN) signaling shifts the balance of

102 his DNA is injected into mice, it stimulates type I interferon (IFN) signaling through a pathway depe

103 ost karyopherin alpha (KPNA) proteins blocks type I interferon (IFN) signaling, which is a central co

104 ke receptor (TLR) 4 signaling and downstream type I interferon (IFN) signaling.

105 is a key negative regulator of RLR-mediated type I interferon (IFN) signaling.

106 n primates and is highly sensitive to mammal type I interferon (IFN) signaling.

107 or of autophagy, but a negative regulator of type I interferon (IFN) signaling.USP19 stabilizes Becli

108 us-prone mice that are prevented by blocking type I interferon (IFN) signalling.

109 een reported in association with recombinant type I interferon (IFN) therapies, with recent concern r

110 aviviruses studied thus far have to overcome type I interferon (IFN) to replicate and cause disease i

111 r T-bet acts as a selective repressor of the type I interferon (IFN) transcriptional program in respo

112 theless, the extent to which Myd88 regulates type I interferon (IFN) versus proinflammatory factors a

113 ents of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analy

114 Importantly, type I interferon (IFN), a major antiviral mediator, als

115 ation, sensitivity to mutagen, inhibition by type I interferon (IFN), and translation efficiency.

116 NS4B-P38G induced lower type I interferon (IFN), IFN-stimulating gene, and proin

117 iral replication coincides with induction of type I interferon (IFN), pro-inflammatory cytokines, and

118 A major arm of cellular innate immunity is type I interferon (IFN), represented by IFN-alpha and IF

119 lls respond to viral infections by producing type I interferon (IFN), which induces the expression of

120 Using established type I interferon (IFN)-deficient mouse models of ZIKV t

121 ISG15 is a type I interferon (IFN)-inducible gene encoding a protei

122 reticulum (ER) stress and production of the type I interferon (IFN)-regulated chemokine CXCL10.

123 ntify a novel role for PRDM16 in suppressing type I interferon (IFN)-stimulated genes (ISGs), includi

124 we noted an increase in the transcription of type I interferon (IFN)-stimulated genes.

125 icles via cytoplasmic RNA sensors to produce type I interferon (IFN).

126 CD95-induced type I interferon (IFN-beta) contributes to the inhibiti

127 Type I interferon (IFN-I) elicits a complex cascade of e

128 deubiquitinase and deISGylase to antagonize type I interferon (IFN-I) immune pathways.

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

130 Type I interferon (IFN-I) led to a downregulation of Sod

131 m dengue virus to ZIKV, antagonizes the host type I interferon (IFN-I) response by preventing JAK-STA

132 us (CMV) infection, leading to a multiphasic type I interferon (IFN-I) response that limits viral rep

133 rica serovar Typhimurium exploits the host's type I interferon (IFN-I) response to induce receptor-in

134 Furthermore, VA1 was sensitive to the type I interferon (IFN-I) response, as VA1 RNA levels we

135 ust virus replication accompanied by delayed type I interferon (IFN-I) signaling orchestrates inflamm

136 antiretroviral therapy (cART), low levels of type I interferon (IFN-I) signaling persist in some indi

137 lymph-borne HSV-1 were permissive only when type I interferon (IFN-I) signaling was blocked; normall

138 as a potent antagonist of the host antiviral type I interferon (IFN-I) system.

139 acytoid dendritic cells (pDCs) are the major type I interferon (IFN-I)-producing cells, and IFN-I act

140 Although type I interferons (IFN) produced in the gut under the i

141 vels of proinflammatory cytokines, including type I interferons (IFN).

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

143 Pretreatment with type I interferons (IFN-alpha and IFN-kappa) increased I

144 Type I interferons (IFN-alpha/beta) and the more recentl

145 ion of toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid de

146 Type I interferons (IFN-I) are critical in antimicrobial

147 be a driving force in immune exhaustion, and type I interferons (IFN-I) are emerging as critical comp

148 naling and promoting efficient production of type I interferons (IFN-I) by myeloid cells.

149 Type I interferons (IFN-Is) are fundamental for antivira

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

151 es we detected a transcriptional response to type I interferons (IFN-Is) in astrocytes during experim

152 ing cascade that results in the induction of type-I interferon (IFN)-dependent responses.

153 Additionally, NLRX1 was observed to reduce type-I interferon (IFN-I) and cytokines in response to H

154 up-regulating antiviral cytokines including type-I interferon (IFN-I).

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

156 omotes dendritic cell maturation by inducing type I interferons (IFNs) and enhances antigen-specific

157 d individuals with malignancies treated with type I interferons (IFNs) and in patients with autoimmun

158 e kinase (RTK) AXL is induced in response to type I interferons (IFNs) and limits their production th

159 ctivates the adaptor protein STING to induce type I interferons (IFNs) and other immune modulatory mo

160 In human blood ex vivo, they induce type I interferons (IFNs) and proinflammatory cytokines:

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

162 Type I interferons (IFNs) are critical antiviral cytokin

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

164 Type I interferons (IFNs) are pleiotropic cytokines well

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

166 Type I interferons (IFNs) play a central role in the imm

167 Interferon regulatory factor 3 (IRF3) and type I interferons (IFNs) protect against infections and

168 in vitro and in vivo, and those neutralizing type I interferons (IFNs) showed a striking inverse corr

169 Type I interferons (IFNs), including IFN-alpha, upregula

170 AcCS were developed for type I interferons (IFNs), which induce cellular activit

171 Viral infection induces production of type I interferons (IFNs), which stimulate the expressio

172 of several stimulatory cytokines, including type I interferons (IFNs).

173 factor 3 (IRF3), resulting in production of type I interferons (IFNs).

174 flammatory cytokines are produced, including type I interferons (IFNs).

175 nd products (RAGE) and induces production of type I interferons (IFNs).

176 Type I interferons (IFNs, including IFN-alphabeta) contr

177 he authors show that the chronic presence of type I interferon in aged mouse brain impedes cognitive

178 for production of inflammatory cytokines and type I interferon in macrophages and dendritic cells (DC

179 cells (pDC) are specialized in secretion of type I interferon in response to pathogens.

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

181 unexpected mechanism underlying the role of type I interferon in the initiation of cognitive impairm

182 syndrome virus (PRRSV) strain A2MC2 induces type I interferons in cultured cells.

183 387 of U-STAT2 might enhance the efficacy of type I interferons in many different clinical settings.

184 n as an endogenous second messenger inducing type I interferons in the cytosolic DNA-sensing pathway.

185 d that the proinflammatory cytokines TNF and type I interferons induced transcriptional cascades that

186 Microbe, Sun et al. (2015) demonstrate that type I interferon induces intestinal epithelial prolifer

187 regulate the transcription of genes encoding type I interferons; instead, it increased the production

188 al up-regulation in many pathways, including type I interferon, interferon gamma, complement activati

189 Type I interferon is a potent substance.

190 ts signaling specificity relative to that of type I interferons is poorly defined.

191 Moreover, exposure of type-I interferon knockout mice to ZIKV results in sever

192 Type I interferon, M2 polarizing genes, and chemokine-ch

193 Because immunomodulatory effects of type I interferon may be a factor in poor T-cell priming

194 duction, transmission, and resolution of the type I interferon-mediated immune response are tightly r

195 to seroconversion, an early potent, largely type I interferon-mediated response correlated with deve

196 Cell-autonomous induction of type I interferon must be stringently regulated.

197 lls in patients with lupus by blocking BAFF, type I interferon, or TLR7 to TLR9.

198 he potentiation of inflammasome responses by type I interferons, particularly in patients with gram-n

199 The STING/type I interferon pathway enhances suppressive inflammat

200 gammaherpesviruses have evolved to usurp the type I interferon pathway to compensate for the decrease

201 ades, including cytokine, innate immune, and type I interferon pathways.

202 Type I interferons potentiated the inflammatory function

203 be, Castiglia et al. (2016) demonstrate that type I interferons produced during Streptococcus pyogene

204 Plasmacytoid dendritic cells (pDC) are type I interferon-producing cells with critical function

205 t upon cGAS-STING.IMPORTANCE By antagonizing type I interferon production and action, many viruses, i

206 cal roles in coordinating both virus-induced type I interferon production and apoptosis; however, the

207 nation, cytokine signaling, protein folding, type I interferon production and complement activation,

208 can be sensed by innate cells, which drives type I interferon production for cross-priming of CD8(+)

209 e, a synthetic analogue of histamine reduces type I interferon production in a mouse model of influen

210 on subsequently results in the inhibition of type I interferon production in the infected cell.

211 e innate response to many pathogens involves type I interferon production that is initiated upon cyto

212 f TRIM29 in airway epithelial cells enhances type I interferon production, and in human nasopharyngea

213 induce production of high concentrations of type I interferon protein in vitro, indicating that host

214 inst homologous virulent virus challenges in type I interferon receptor (IFNAR)-knockout mice.

215 inhibit Tyk2-dependent signaling through the Type I interferon receptor but not Tyk2-independent sign

216 We found that downregulation of the type I interferon receptor chain IFNAR1 occurs in human

217 e the neuropathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-)

218 et al. describe tumor-induced degradation of type I interferon receptor IFNAR1 chain as a new immune-

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

220 re we found that deficiency in signaling via type I interferon receptor led to deregulated activation

221 STATs 1 and 2, transmits the signal from the type I interferon receptor to the genome.

222 Using mice that lack the type I interferon receptor, we examined sexual transmiss

223 on of this DDR depends on signaling from the type I interferon receptor.

224 However, the type I interferon regulator IRF1, kappa interferon (IFN-

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

226 nterferon genes (STING) is essential for the type I interferon response against DNA pathogens.

227 as important host effector molecules of the type I interferon response against viruses.

228 This is coincident with induction of a type I interferon response and apoptosis through the dsR

229 ing of double-stranded RNA (dsRNA) causing a type I interferon response and apoptosis.

230 onstrated impaired viral clearance, a slower type I interferon response and delayed production of vir

231 Additionally, the type I interferon response and sex hormones alter both C

232 Additionally, we found that the type I interferon response and sex hormones can alter bo

233 ly, our data suggest that, although an early type I interferon response appears to be crucial to cont

234 edary viruses were as sensitive to the human type I interferon response as HCoV-229E.

235 ranscript abundance and association with the Type I interferon response in an SIV model.

236 stealthy, since the infection rarely induces type I interferon response in the early phase.

237 d antiviral drug ganciclovir (GCV) induces a type I interferon response independent of its canonical

238 ed fewer symptoms had not only a more modest type I interferon response initially, but also a protrac

239 ines including IL-1beta, while the antiviral type I Interferon response is not triggered in these cel

240 S-deficient Chlamydia induced an exacerbated type I interferon response that required the host cGAS/S

241 Cell-autonomous cytotoxicity of type I interferon response via induction of endoplasmic

242 -rich extracellular vesicles, which induce a type I interferon response via the Toll-like receptors-M

243 TING variants that constitutively induce the type I interferon response were found in patients with a

244 One such pathway, the type I interferon response, recognizes viral or mitochon

245 ntifies POLA1 as a critical regulator of the type I interferon response.

246 cinia virus B19 protein, an inhibitor of the type I interferon response.

247 es palmitoylation of STING and abolishes the type I interferon response.

248 le strategies to avoid the activation of the type I interferon response.

249 through induction of a microbiota-dependent type I interferon response.

250 te to prevent the spurious activation of the type I interferon response.

251 taG-H5N1, and VLV in the adult brain was the type I interferon response; all three viruses were letha

252 the culture supernatant by activation of the type I interferon-response pathway.

253 feron-stimulated gene expression, potentiate type I interferon responses and confer broad viral resis

254 t the capacity of HAV to evade MAVS-mediated type I interferon responses defines its host species ran

255 ess, which enhances antiviral signalling and type I interferon responses during infection.

256 rCl-13, yet the two viruses induced similar type I interferon responses in mice.

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

258 pattern recognition receptors that activate type I interferon responses, which establish an antivira

259 consistently antagonize signaling related to type I interferon responses.

260 load, markers of macrophage activation, and type I interferon responses.

261 oluble cGAMP, the Ace-DEX cGAMP MPs enhanced type-I interferon responses nearly 1000-fold in vitro an

262 Type I interferon restrains interleukin-1beta (IL-1beta)

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

264 the observed neurotoxicity through increased type I interferon secretion.

265 Type I interferons serve as the first line of defense ag

266 Female mice lacking type I interferon signaling (Ifnar1(-/-)) crossed to wil

267 erm-free mice, revealing essential roles for type I interferon signaling and microbiota in H polygyru

268 Here we identify type I interferon signaling as a key inducer of a known

269 Further, we demonstrate that type I interferon signaling counteracts the antiviral ef

270 tures in viral RNAs as foreign to initiate a Type I interferon signaling response.

271 re also characterized by an up-regulation of type I interferon signaling suggests the possibility tha

272 cGAMP-independent constitutive activation of type I interferon signaling through TBK1 (TANK-binding k

273 in replication complexes, thereby inhibiting type I interferon signaling.

274 A set of 145 cis-eQTLs depended on type I interferon signaling.

275 es toward an anti-inflammatory phenotype via type I interferon signaling.

276 h functional importance in the regulation of type I interferon signaling.

277 s with HAP demonstrated underexpression of a type-I interferon signaling gene signature.

278 also predicted a central role for decreased type-I interferon signaling.

279 In conclusion, we demonstrate that type I interferon signalling in CD8(+) T cells drives Eo

280 T cells are strongly affected in absence of type I interferon signalling.

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

282 toantibodies (including anti-DNA IgG), and a type I interferon signature.

283 aracterized by autoantibody production and a type I interferon signature.

284 presentation while simultaneously activating type I interferon-stimulated genes.

285 one of the most strongly induced genes after type I interferon stimulation, analysis of ISG15 functio

286 T946) displayed enhanced basal expression of type I interferons, survived a lethal viral challenge an

287 rategically target crucial components of the type I interferon system.

288 showed that DC are the primary producers of type I interferons (T1-IFN), requisite cytokines for sur

289 s more sensitive to the antiviral effects of type I interferon than other known human-pathogenic flav

290 ons; instead, it increased the production of type I interferons through an epigenetic mechanism by ma

291 Although type I interferon transcription decreased in MDA5(-/-) m

292 cell inflammation," including IRF8-dependent type I interferon transcriptional signatures and T-cell

293 ta levels are associated with the outcome of type I interferon treatment of CHB patients.

294 d out of the context of the infection blocks type I interferon triggered by STING stimuli, through th

295 nmt3a selectively impaired the production of type I interferons triggered by pattern-recognition rece

296 ous manifestations, along with activation of type I interferon, underlines the systemic nature of fam

297 Whereas IFN-gamma was essential, endogenous type I interferons were insufficient to prime caspase-11

298 Interestingly, neutrophils responded to Type I interferons, whereas they both produced and respo

299 R-31 increased the sensitivity of T cells to type I interferons, which interfered with effector T cel

300 in macaque astrocytes and further induced by Type I interferon, while IFN produced a weaker response