ライフサイエンスコーパス: IFN

1 IFN regulatory factor 3 (IRF3) is a transcription factor

2 IFN-alpha/-beta have very low basal expression levels bu

3 IFN-beta and other IFN-related and neuroinflammatory gen

4 IFN-beta did not induce inflammatory cytokine production

5 IFN-beta is a key component of the innate immune respons

6 IFN-gamma binds to its receptor on Leishmania-infected m

7 IFN-lambda responses to dsRNA in the human infant airway

8 IFN-lambda1 is a key placental IFN that appeared less pr

9 IFNs, produced during viral infections, induce the expre

10 These findings identify an IL-36/ IFN-I axis contributing to extracutaneous inflammation i

11 signal through the MAVS adaptor to activate IFN responses against viruses.

12 7 (TLR7) agonist imiquimod (IMQ) to activate IFN-sensitive gene (ISG) pathways and induce psoriasifor

13 more, inhibition of ERK1/2 kinases activates IFN-kappa expression.

14 minescence-based assay was developed against IFN-gamma and provided an optimized, physiologically rel

15 ated by others and us that interferon alpha (IFN-alpha) treatment of hepatocytes induced a prolonged

16 Interferon-alpha (IFN-alpha) can suppress production of T-cell polarizing

17 leukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-beta, and TNF-alpha mRNA levels induced by Sendai vi

18 Although IFN-gamma typically helps microbial clearance, we found

19 G or beta-glucan, Mtb reprograms HSCs via an IFN-I response that suppresses myelopoiesis and impairs

20 eased splenic Tregs producing both IL-10 and IFN-gamma 8-fold (p < 0.005) compared to LL-vehicle trea

21 ion in lungs including TNF, IL-6, IL-10, and IFN-gamma.

22 nd T cells, respectively, restored IL-12 and IFN-gamma cytokine levels and BMM -T cell interaction.

23 gulate T-bet and coexpress IL-17, IL-22, and IFN-gamma in a STAT3- and retinoic acid-dependent manner

24 ted with decreased articular IL-12/23p40 and IFN-gamma levels.

25 es toll-like receptor (TLR)-9 activation and IFN-alpha production.

26 d that only the combination of TNF-alpha and IFN-gamma induced inflammatory cell death characterized

27 eutralizing antibodies against TNF-alpha and IFN-gamma protected mice from mortality during SARS-CoV-

28 HSV DNA copies, and surges in granzyme B and IFN-gamma occurred within the early hours after reactiva

29 interactions between the IFN-alpha/beta and IFN-gamma pathways in achieving optimal antiviral respon

30 communication between the IFN-alpha/beta and IFN-gamma signaling pathways to optimize antiviral IFN-g

31 MAIT, and Vdelta2(+) gammadelta T cells) and IFN-gamma production by them, with mycobacterium-specifi

32 Ks and STATs and their roles in cytokine and IFN action represented a significant basic advance and a

33 s, 107 each were treated with fingolimod and IFN beta-1a for up to 2 years.

34 cognition receptors, MHC class II genes, and IFN-gamma-induced GTPases, with antimicrobial function.

35 IRF5(13,14), and are controlled by IFN-I and IFN-gamma in vivo(15-17).

36 nteracted with key proteins in NF-kappaB and IFN-I pathways in cells.

37 lation of the IL-2/STAT5, TNF/NF-kappaB, and IFN-gamma signaling pathways.

38 correlation with cell adhesion molecules and IFN response pathways and a strong negative correlation

39 However, the link between COPA mutations and IFN signaling is unknown.

40 Furthermore, the combination of MTP-PE and IFN-gamma on AML blasts generated an inflammatory cytoki

41 estored mitochondrial membrane potential and IFN-gamma production.

42 acy (antigen-specific antibody responses and IFN-gamma production) and biodistribution (antigen and a

43 d progenitors revealed a decrease in TLR and IFN signaling.

44 Anti-IFN-gamma autoantibody levels were measured in plasma sa

45 protein, as evidenced by an observed hd-anti-IFN-gamma-induced increase in the specific binding of IF

46 iral accessory protein Orf6 exerts this anti-IFN activity.

47 mma signaling pathways to optimize antiviral IFN-gamma activity.

48 ) and interleukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-beta, and TNF-alpha mRNA levels induced b

49 nscription activity and partially attenuated IFN-alpha suppression of cccDNA transcription.

50 Augmented IFN-gamma responses in the HDM allergic airway disease m

51 which can exploit the inflammasome to avoid IFN-I(12), are restricted by IFN-I via IRF5(13,14), and

52 L1 signaling also induced an anergic T-bet(-)IFN-gamma(-) phenotype in CD8(+) T cells and was equally

53 in cells prestimulated with interferon beta (IFN-beta), we identified a small number of factors requi

54 dited Alu RNAs are potent activators of both IFN and NF-kappaB responses via the dsRNA sensors, RIG-I

55 Here, we show that both IFN-gamma stimulation and murine norovirus (MNV) infecti

56 high cellular responses, as characterized by IFN-gamma production, upon re-stimulation with SARS-CoV-

57 IFN-I via IRF5(13,14), and are controlled by IFN-I and IFN-gamma in vivo(15-17).

58 om latently infected humans, as evidenced by IFN-gamma release upon peptide stimulation.

59 not inhibit STAT1 phosphorylation induced by IFN-gamma.

60 ntial cell death that is in part mediated by IFN-independent activities of STING.

61 contrast, SARS-CoV-1 was restricted only by IFN-alpha in these cell lines.

62 masome to avoid IFN-I(12), are restricted by IFN-I via IRF5(13,14), and are controlled by IFN-I and I

63 DSG3 autoantibodies stimulated DSG3-CAART IFN-gamma secretion and homotypic clustering, consistent

64 change in expression levels of GzmB, CD107a, IFN-gamma, and TNF was examined.

65 In contrast, IFN-gamma response via TCR and plasma IgG specific for B

66 f the ability of ISG15/USP18 axis to control IFN-I signaling and reveal the therapeutic potential of

67 person-year among patients treated with DAA, IFN, and antiviral naive, respectively (P < 0.001).

68 molecule PF-74 also induced a cGAS-dependent IFN response.

69 Furthermore, the MDA5/MAVS-dependent IFN response was critical for the induction of optimal a

70 nd silencing of COPA induced STING-dependent IFN signaling.

71 NRF2 agonists 4-OI and DMF induce a distinct IFN-independent antiviral program that is broadly effect

72 ast, alveolospheres pretreated with low-dose IFNs show a reduction in viral replication, suggesting t

73 the antagonistic caspase that downregulates IFN-I production.

74 Among survivors, early IFN-alpha2b was not associated with hospital discharge o

75 own that this depends on PLP-CD8 elaborating IFN-gamma and perforin in a coordinated suppression prog

76 bers of tumor-infiltrating T cells, elevated IFN signaling, and immune checkpoint expression, as well

77 ulatory inflammatory cytokines, for example, IFN-gamma and IL-12, in CCR2i- versus vehicle-treated mi

78 As expected, IFN-gamma induced genes involved in Ag presentation and

79 assays indicated that GBP2 is important for IFN-gamma-dependent anti-MNV activity in murine macropha

80 ta provide insight into the requirements for IFN-gamma production and how IFN-gamma enhances local im

81 together, we uncover a nonredundant role for IFN-gamma and its downstream signaling molecules STAT1 a

82 Here, we identify a nonredundant role for IFN-lambda in immune dysregulation and tissue inflammati

83 -T cell activation through interferon gamma (IFN-gamma) production and CD107a membrane accumulation b

84 he natural history of anti-interferon-gamma (IFN-gamma) autoantibody-associated immunodeficiency synd

85 at T cell infiltration and interferon-gamma (IFN-gamma) signaling signatures correspond most highly w

86 bjects with RSV infection showed the highest IFN-lambda airway levels; and (c) individuals with the h

87 equirements for IFN-gamma production and how IFN-gamma enhances local immune responses to prevent Bp-

88 isplayed significant up-regulation of type I IFN (IFN)-stimulated genes (ISGs).

89 Type I IFN (IFN-I) is thought to be rapidly internalized and de

90 hage death is dependent on the host's type I IFN (IFN-I) response.

91 Moreover, type I IFN alone was sufficient to induce cytokine and chemokin

92 f IFN-stimulated genes in response to type I IFN and leads to 1) promotion of cell-to-cell spread by

93 and the response of IEC organoids to type I IFN is strikingly increased in magnitude and scope relat

94 ition of IFN-beta, a key component of type I IFN mechanisms to address its role in TBI pathophysiolog

95 enic patients and decreased following type I IFN neutralisation with anifrolumab in the SLE phase IIb

96 oles on goblet cells do not depend on type I IFN or on IL-22 signaling, pathways responsible for prot

97 ine phosphorylation induced either by type I IFN or overexpressed Jak1, paralleling MARV VP40.

98 , mRNA and protein expressions of the type I IFN pathway were downregulated under hypoxic conditions.

99 relationship between hypoxia and the type I IFN pathway, which comprises the sensing of double-stran

100 genous activation of six genes in the type I IFN pathway.

101 death, we reveal that IFN-lambda and type I IFN production were both diminished and delayed, induced

102 motes phagosomal permeabilization and type I IFN production, key features of tuberculosis pathogenesi

103 f IFN genes (STING) pathway to induce type I IFN production.

104 oids have increased expression of the type I IFN receptor relative to neonate IECs, and the response

105 virus levels after ZIKV challenge in type I IFN receptor-deficient mice and wildtype mice administer

106 administered neutralizing Abs against type I IFN receptor.

107 viral HA-induced degradation of host type I IFN receptor.

108 nt with a defect in resolution of the type I IFN response, Trim14 knockout macrophages have more phos

109 enes spread through modulation of the type I IFN response, which is known to be exploited by L. monoc

110 tion of endosomal pH to ensure strong type I IFN secretion exclusively during infection, avoiding aut

111 elating with mitochondrial abundance, type I IFN signaling and effector immunity.

112 Type I IFN signaling caused tight junction dysregulation in IEC

113 rough adulthood, and requires ongoing type I IFN signaling to maintain it.

114 of LGP2, MDA5-mediated activation of type I IFN signaling was abrogated.

115 in BAFF expression were dependent on type I IFN signaling.

116 nterferon regulatory factor-dependent type I IFN synthesis followed by JAK/STAT-dependent interferon-

117 y capable of producing high levels of type I IFN, but rapidly lost this capacity, even before the vir

118 Type I IFN-mediated JAK-STAT signaling is severely impaired, an

119 r motifs, whereas the expanded set of type I IFN-specific ISGs, including proapoptotic genes, have we

120 The expanded type I IFN-specific response includes proapoptotic genes and po

121 tion in a plasmacytoid dendritic cell-type I IFN-T/B lymphocyte network.

122 e for STING activation was to produce type I IFN.

123 -6258 induced a potent cGAS-dependent type-I IFN response in tumor cells, increased IFNgamma-producin

124 ndritic cells (pDCs) produce abundant type I IFNs (IFN-I) in response to viral nucleic acids.

125 Interestingly, induction of type I IFNs after A. fumigatus challenge was only partially dep

126 Type I IFNs play a complex role in determining the fate of micr

127 Endogenous release of type I IFNs with the double-stranded RNA mimetic poly(I:C) like

128 In our efforts to identify IFN-induced cellular proteins that mediate the suppressi

129 yed significant up-regulation of type I IFN (IFN)-stimulated genes (ISGs).

130 Type I IFN (IFN-I) is thought to be rapidly internalized and degrade

131 death is dependent on the host's type I IFN (IFN-I) response.

132 c cells (pDCs) produce abundant type I IFNs (IFN-I) in response to viral nucleic acids.

133 were associated with impaired type I and II IFN responses.

134 We previously reported that type I and II IFNs control MuPyV infection in non-central nervous syst

135 B. pertussis-infected mice, lung type I/III IFN responses correlated with increased proinflammatory

136 is end, mice deficient in type I, II, or III IFN receptors or STAT1 were infected intracerebrally wit

137 ially the less adverse effect-prone type III IFN are good candidates for the management of COVID-19.

138 ent on MDA5/MAVS signaling, whereas type III IFN expression was entirely dependent on MDA5/MAVS signa

139 IECs) are particularly dependent on type III IFN for the control and clearance of virus infection, bu

140 ferential responsiveness of IECs to type III IFN in vivo enables selective ISG expression during infe

141 expression that mirrors the in vivo type III IFN response.

142 tro treatment of IEC organoids with type III IFN results in ISG expression that mirrors the in vivo t

143 in magnitude and scope relative to type III IFN.

144 ISGs stimulated in common by type I and III IFNs have strong interferon-stimulated response element

145 atment and posttreatment with type I and III IFNs significantly reduced virus replication in pHAE cul

146 report in Science that type III IFNs disrupt epithelial cell proliferation and different

147 mouse cell lines through type I and type III IFNs.

148 isk factors, but these cells showed impaired IFN-gamma production.

149 eving optimal antiviral responses.IMPORTANCE IFN-alpha/beta induction limits CNS viral spread by esta

150 In IFN-gamma(-/-) mice, there is deficient granuloma format

151 of WT mice, whereas levels were mitigated in IFN-beta(-/-) mice.

152 ly, there is a reduction in cytosolic Trp in IFN-gamma-activated host cells.

153 Mice lacking NFAT5 exhibit increased IFN-I production and better control of viral burden upon

154 -of-function genetic screening of individual IFN-stimulated genes (ISGs) on hepadnaviral mRNAs transc

155 Staphylococcus aureus, known to induce IFN production, could play a role in cutaneous inflammat

156 nfants (<18 months) had higher virus-induced IFN-lambda airway secretion; (b) subjects with RSV infec

157 ) individuals with the highest virus-induced IFN-lambda levels (>90th percentile) had higher viral lo

158 on in the spleens and livers of STm-infected IFN-gamma(-/-) and T-bet(-/-) mice.

159 bgroups for further investigation of inhaled IFN-beta1a.

160 ilarly to WT, infection with W105A inhibited IFN/ISG expression despite displaying an attenuated phen

161 Interferon (IFN)-Is are crucial mediators of antiviral immunity and

162 AVS) protein-dependent antiviral interferon (IFN) responses.

163 Alpha/beta interferon (IFN-alpha/beta) signaling through the IFN-alpha/beta rec

164 ave shown previously that type I interferon (IFN) contributes to the pathogenesis of this disease.

165 d disease, which requires type I interferon (IFN) receptor signaling, TLR9-driven fatality is depende

166 Type I interferon (IFN) response is commonly recognized as the main signali

167 eted increased amounts of type I interferon (IFN), which could be limited by CGAS or STING knockdown,

168 18, a potent inhibitor of type I interferon (IFN)-I.

169 and Zika virus through a type I interferon (IFN)-independent mechanism.

170 ng to investigate how the type I interferon (IFN)-responsive regulatory network operates in single hu

171 ts systemic production of type I interferon (IFN).

172 id dendritic cells-(pDCs)-Type I interferon (IFN-I) and acts as autoantigen for pathogenic Th17-cells

173 itic cells (pDCs) produce type I interferon (IFN-I) and are traditionally defined as being BDCA-2+CD1

174 F3 (not TBK1) and enhance type I interferon (IFN-I) production in macrophages.

175 this report, we evaluate type I interferon (IFN-I) sensitivity of SARS-CoV-2 relative to the origina

176 e bone marrow (BM) via a type II interferon (IFN-II) or interleukin-1 (IL1) response, respectively, w

177 hy had antibody that neutralized interferon (IFN)-alpha, but not IFN-gamma.

178 rrespondingly, the expression of interferon (IFN)-responsive genes (IRGs) in cells and in mice was po

179 CV infections stimulate a robust interferon (IFN) response in a retinoic acid-inducible gene I (RIG-I

180 Here, we report that interferon (IFN) signals convey resistance to CDC-induced pores on m

181 d in the expression of type III interferons (IFN-lambda).

182 bal threat, type I and type III interferons (IFNs) are currently being evaluated for their efficacy.

183 lls, and ultimately requires tumor-intrinsic IFN-gamma signaling, via a mechanism that is distinct fr

184 cies (ROS) levels are elevated, mTOR and IRF/IFN-beta signaling pathways are enhanced, leading to cel

185 mography (CT) scan improvement, whereas late IFN-alpha2b was associated with delayed recovery.

186 RNA sequencing, we found that in GA lesions IFN-gamma production by CD4(+) T cells is upregulated an

187 lysine methylation/demethylation of M(LPS + IFN-gamma)/M(IL-10) genes is one of the factors that dir

188 Twice as many IFN beta-1a-treated than fingolimod-treated patients had

189 d apply protein correlation profiling to map IFN-induced rearrangements in the human protein-protein

190 12 induction in macrophages & STAT4-mediated IFN-gamma synthesis in T cells.

191 over, we documented that cGAS-STING-mediated IFN production is mediated by nuclear translocation of I

192 ion of cGAS-STING dampened the TLR9-mediated IFN production.

193 well as TNF-alpha, IL-6, or IL-17A, but not IFN-gamma, similarly induced sHLH in SIRPalpha(-/-) mice

194 neutralized interferon (IFN)-alpha, but not IFN-gamma.

195 ithelial cultures, we observe the absence of IFN-I stimulation by SARS-CoV-2 alone but detect the fai

196 mor eradication related to the activation of IFN-gamma-producing CD8 T cells.

197 secretion and transcriptional activation of IFN-stimulated genes (ISG).

198 -induced increase in the specific binding of IFN-gamma to its receptor in U937 cells, enhanced induce

199 Blockade of IFN-gamma signaling in mice increases lesion size and pa

200 hich was reversed by therapeutic blockade of IFN-gamma.

201 s substantially attenuated in the context of IFN-I pretreatment, whereas SARS-CoV is not.

202 teomic approaches to describe the effects of IFN signaling on the human proteome, and apply protein c

203 The restrictive effects of IFN-I require the interferon regulatory factor IRF5, whi

204 ly of its ability to block the expression of IFN and ISG mRNA.

205 t is associated with increased expression of IFN-beta and other IFN-related genes.

206 atterns (e.g., dsRNA) activate expression of IFN-stimulated genes (ISGs), which protect hosts from in

207 eficiency results in increased expression of IFN-stimulated genes in response to type I IFN and leads

208 ctions, induce the expression of hundreds of IFN-stimulated genes (ISGs).

209 eak may be related to the lower induction of IFN-beta.

210 Inhibition of IFN-beta signaling resulted in reduced neuroinflammation

211 of genetic or pharmacological inhibition of IFN-beta, a key component of type I IFN mechanisms to ad

212 trast, TDM/TDB exerted delayed inhibition of IFN-gamma-induced genes, including pattern recognition r

213 Moreover, ruxolitinib, an inhibitor of IFN-triggered Janus kinase/signal transducer and activat

214 ry environment resulted in reduced levels of IFN dependent chemokines Rantes (CCL5) and CXCL10.

215 he 2014-15 outbreak induced higher levels of IFN-beta despite relatively minor differences in replica

216 Neutralization of IFN-gamma during infection abrogated Ido1 expression and

217 However, the percentage of IFN-gamma(+) ILCs in infected colons was 5- to 10-fold h

218 The results reveal how perturbation of IFN-alpha/beta signaling in neurons can worsen disease c

219 ds to activity-associated phosphorylation of IFN regulatory factor-3.

220 correlated with decreased phosphorylation of IFN regulatory factory 7 (IRF7) and NF-kappaB.

221 e before ND PIV5 can block the production of IFN, we demonstrate that the converse is also true, i.e.

222 n U937 cells, enhanced induced production of IFN-gamma in human PBMC culture, and increased survival

223 ocytic host cell reservoir via regulation of IFN-gamma and IL-10.

224 NK cells were the main source of IFN-gamma production, which was enhanced by IL-15.

225 The provision of a source of IFN-gamma reverses this, coincident with subsequent gran

226 NK cells are likely key sources of IFN-gamma in this model.

227 mpared with mice deficient in all sources of IFN-gamma.

228 ic GMP-AMP synthase (cGAS) and stimulator of IFN genes (STING) pathway to induce type I IFN productio

229 the antiviral adaptor protein, stimulator of IFN genes.

230 These results do not support the use of IFN-beta-1a in the management of ARDS.

231 trains is sensitive to exogenous addition of IFNs, suggesting the potential of IFNs as therapeutics.

232 suggesting the prophylactic effectiveness of IFNs against SARS-CoV-2.

233 ddition of IFNs, suggesting the potential of IFNs as therapeutics.

234 naling, TLR9-driven fatality is dependent on IFN-gamma receptor signaling.

235 pective of CEBPB, miR-520G overexpression or IFN-gamma treatment.

236 IFN-beta and other IFN-related and neuroinflammatory genes were also upregu

237 h increased expression of IFN-beta and other IFN-related genes.

238 cells to suppress an atypical and pathogenic IFN-gamma response to inhaled HDM.

239 n hours of infection through a bile acid-pDC-IFN signaling axis, which affects viremia, dissemination

240 F)/ribavirin (RBV)/pegylated interferon (PEG-IFN), 25.2%; SOF/RBV, 62.4%; SOF/RBV/daclatasavir (DCV),

241 s and supports the clinical use of pegylated IFN-lambda1a as a treatment for human COVID-19(6).

242 IFN-lambda1 is a key placental IFN that appeared less protective than IFN-alpha, sugges

243 Circulating plasma IFN-gamma levels were also assayed in 400 patients with

244 al clearance, we found that increased plasma IFN-gamma in early clinical sepsis was associated with t

245 pitopes, induced HSV-specific polyfunctional IFN-gamma-producing CD107(ab+) CD4(+) T cells associated

246 ) cells in Rag-deficient mice both prevented IFN-gamma production and rescued mutant colonization.

247 mphoblast expansion and cytokine production (IFN-gamma, IL-2, and TNF), with the highest median magni

248 in single human cells to process repetitive IFN stimulation.

249 Conversely, selective IFN receptor blockade effectively diminished the ongoing

250 ut the physiological basis of this selective IFN response is not well understood.

251 uction by them, with mycobacterium-specific, IFN-gamma-producing, purely adaptive CD8(+) alphabeta T,

252 T cell to combined CD4 Th1/Th2 cell subsets (IFN-gammaCD4 and IL-4CD4 cells; P = 0.0001) compared to

253 bilization of its putative protein substrate IFN-gamma receptor 1 (IFNGR1) at the protein level in TN

254 By investigating temporal IFN and inflammatory cytokine patterns in 32 moderate-to

255 ental IFN that appeared less protective than IFN-alpha, suggesting a potential weakness in antiviral

256 (+) cells produce helper cytokines, and that IFN-gamma(+) cells produce cytotoxic molecules.

257 We have recently demonstrated that IFN regulatory factor (IRF) 8 was dispensable for caspas

258 espiratory failure and death, we reveal that IFN-lambda and type I IFN production were both diminishe

259 Gene expression interrogation revealed that IFN pathway was grossly upregulated in clinical AD and s

260 efective (ND) virus genomes and activate the IFN-induction cascade before ND PIV5 can block the produ

261 an block the ability of DVGs to activate the IFN-induction cascade.

262 diminished the accumulation of dsRNA and the IFN response in JUNV-infected cells.

263 and disrupt complex interactions between the IFN-alpha/beta and IFN-gamma pathways in achieving optim

264 tightly regulated communication between the IFN-alpha/beta and IFN-gamma signaling pathways to optim

265 -mediated inflammatory process driven by the IFN-gamma pathway.

266 er, the virus rapidly evolves to exploit the IFN-alpha response for its replication, spread, and path

267 aling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells.

268 lation of T cell-derived IL-10 increased the IFN-gamma and IL-17A response to HDM, reducing IL-13 lev

269 f RNAs can also engage RLRs and modulate the IFN-I response, indicating that the distinction between

270 cell protein (ICP)0 and key elements of the IFN pathway to identify possible novel targets that cont

271 r, HPV16 integrated into the promoter of the IFN regulatory factor 4 (IRF4) gene, which plays an impo

272 s an important role in the regulation of the IFN response to viral infection.

273 o cccDNA minichromosomes and phenocopied the IFN-alpha-induced posttranslational modifications of ccc

274 In patients with RA, the IFN signature is characterised by up-regulation of SIGLE

275 Therapies targeting the IFN family and T-cell-activating factors may therefore b

276 feron (IFN-alpha/beta) signaling through the IFN-alpha/beta receptor (IFNAR) is essential to limit vi

277 that STING controls HSV-1 infection through IFN-independent activities.

278 roximal complex is assembled upon binding to IFN is poorly understood.

279 enic viruses have evolved countermeasures to IFN-I restriction, and genetic loss of viral IFN-I antag

280 hey are largely dormant functionally, due to IFN-I-induced negative regulators.

281 rient when the human host cell is exposed to IFN-gamma.

282 CoV, the novel CoV is much more sensitive to IFN-I.

283 these data suggest that chronic exposure to IFNs induces barrier disruption that allows for higher S

284 Traf3ip3 have increased RNA virus-triggered IFN-I production and reduced susceptibility to virus.

285 In turn, IFN-gamma released by Vdelta2(+) cells upregulates IL-12

286 FOXP3/IL2-, inflammation- and finally type1 IFN-signalling subnetworks, forming a single highly inte

287 ibroblasts (MEFs), and human HeLa cells upon IFN stimulation.

288 ure to counteract STAT1 phosphorylation upon IFN-I pretreatment, resulting in near ablation of SARS-C

289 sive CD8(+) T-cell clones was measured using IFN-gamma ELIspot.

290 t of chronic Chagas' disease patients, using IFN-gamma secretion as a readout.

291 onsistent control of disease activity versus IFN beta-1a (including treatment-naive and younger patie

292 IFN-I restriction, and genetic loss of viral IFN-I antagonists leads to virus attenuation.

293 s were dependent on IL-18 and IL-12, whereas IFN-gamma secretion was restricted by high concentration

294 It will be worth investigating whether IFN-gamma-producing ILCs also improve endometrial resist

295 suggested that T1 CRSsNP was associated with IFN-gamma signaling and antiviral immunity controlled by

296 1458 and rs3902920 in GSDMB colocalized with IFN regulatory factor binding sites and associated with

297 lipopolysaccharide (LPS) in combination with IFN-gamma inhibited PINK1-dependent mitophagy in macroph

298 Treating HBV infection, either with IFN or NUCs, substantially reduces the risk of HCC devel

299 attenuates disease only in mice treated with IFN-I.

300 e, Th1 cells act to restrict bacteria within IFN-gamma-dependent iNOS(+) granulomas and prevent disse