ライフサイエンスコーパス: IFN-beta

1 IFN-beta + NAg in Alum vaccination elicited elevated num

2 IFN-beta and IFN-alpha1, -2, and -8 were induced in an I

3 IFN-beta and MOG35-55 elicited suppressive FOXP3(+) Treg

4 IFN-beta inhibited replication of A2 and A2(91G) in vitr

5 IFN-beta injections induced BAFF expression mainly in ne

6 IFN-beta is widely used in the treatment of multiple scl

7 IFN-beta production relied mainly on the activation of t

8 IFN-beta significantly suppressed GM-CSF production by T

9 IFN-beta treatment increases the absolute number of regu

10 IFN-beta treatment increases transitional and regulatory

11 IFN-beta-producing pDCs exhibit a distinct transcriptome

12 IFN-beta/Alum-based vaccination exhibited hallmarks of i

13 ogated in mice treated with exogenous type 1 IFN-beta.

14 urified malaria pigment with DNase abrogated IFN-beta induction.

15 These findings that BBI could activate IFN-beta-mediated signaling pathway, initialize the intr

16 STING such as 2',3'-cGAMP and also activated IFN-beta and ISG expression; and (v) UL46 binds to both

17 dition to its well-known signaling activity, IFN-beta may be directly antimicrobial and be part of a

18 er TLR9 stimulation and only weakly affected IFN-beta and IL-12p40 production.

19 acologically downregulated without affecting IFN-beta.

20 n virus induction of interferon (IFN)-alpha, IFN-beta and IFN-lambda in bronchial epithelial and bron

21 Here we show that in addition to IFN-alpha, IFN-beta and IL-27 also affect Vpu-mediated BST-2 downre

22 arly, the levels of Gal-9, Tim-3, IFN-alpha, IFN-beta, IFN-gamma, and IL-10 were all significantly in

23 fection, and the levels of CD137, IFN-alpha, IFN-beta, IFN-gamma, IL-4, and IL-10 in the lungs were a

24 induces expression of type I IFNs (IFN-alpha/IFN-beta) during infection.

25 infection, consistent with the results of an IFN-beta promoter reporter assay suggesting that all tPs

26 a gene expression, and in the presence of an IFN-beta-mediated antiviral state, ExoN(-) viral RNA lev

27 ent-derived TNBC tumors demonstrates that an IFN-beta metagene signature correlates with improved pat

28 Treatment with an IFN-beta receptor blocking antibody or knockdown of IFN-

29 the expression of TLR9-induced IL-12p40 and IFN-beta, but not of IL-10.

30 1 increase NK cell cytotoxicity by IL-23 and IFN-beta-dependent upregulation of NKG2D, IL-1beta-depen

31 roduced high amounts of type I IFN-alpha and IFN-beta (IFN-alpha/beta) in the serum and were resistan

32 ering RNA primarily suppressed IFN-alpha and IFN-beta levels during infection of allergic mice.

33 blood cells in vitro; but only IFN-alpha and IFN-beta were significantly increased after alpha-lactos

34 logous to that of type I IFNs (IFN-alpha and IFN-beta) via the induction of IFN-stimulated genes (ISG

35 Along with IFN-alpha and IFN-beta, IFN-gamma was demonstrated to control filoviru

36 ng to induce the expression of IFN-alpha and IFN-beta, respectively.

37 terferon (IFN), represented by IFN-alpha and IFN-beta.

38 lls ectopically expressing bat IFN-alpha and IFN-beta.

39 e cytokines interferon-alpha (IFN-alpha) and IFN-beta prevented the systemic spread of murine norovir

40 n produced for clinical use, IFN-alpha2a and IFN-beta, were compared for activity in protecting human

41 Type 1 IFNs, including the IFN-alphas and IFN-beta, activate the interferon-alpha/beta receptor (I

42 lls in PB compared with healthy controls and IFN-beta-treated MS patients.

43 the expression of inflammatory cytokines and IFN-beta.

44 ncreasing IFN-stimulated gene expression and IFN-beta/lambda.

45 Using IFNAR1 and IFN-beta variants, we show that this interface contribut

46 the inhibition of the activation of IRF3 and IFN-beta transcription in Ud virus-infected cells.

47 has no effect on the activation of IRF3 and IFN-beta transcription.

48 ession of IFN regulatory factor 7 (IRF7) and IFN-beta, as well as increased nuclear exclusion of FOXO

49 VS-associated IRF3 and induction of MAVS and IFN-beta gene signatures.

50 cterial RNA with secretion of IL-6, TNF, and IFN-beta, which is critically dependent on lysosomal mat

51 1 signaling, IRF3 nuclear translocation, and IFN-beta production.

52 e NS3/4A, which efficiently cleaves TRIF and IFN-beta promoter stimulator 1, adaptors for TLR3 and th

53 re characterized in samples of untreated and IFN-beta-treated MS patients versus healthy subjects.

54 tructural protein 1 (NS1) of WNV antagonizes IFN-beta production, most likely through suppression of

55 echanism that serves to degrade an antiviral IFN-beta effector is exploited by HSV-1 to establish an

56 s dual roles in the suppression of antiviral IFN-beta induction as well as the promotion of proinflam

57 several type I IFN-associated genes, such as IFN-beta and guanylate-binding proteins (GBPs), are down

58 phages, impairing their ability to attenuate IFN-beta production and acquire an M2-like hyporesponsiv

59 dary TLR3-response genes requiring autocrine IFN-beta stimulation.

60 macrophages is necessary for governing basal IFN-beta expression, as well as the magnitude of IFN-bet

61 wed improved inhibition of viral dsRNA-based IFN-beta induction.

62 d hallmarks of infectious tolerance, because IFN-beta + OVA in Alum-specific vaccination inhibited EA

63 Treatment with IFN-beta (IFN-beta) led to a less aggressive epithelial/non-CSC-li

64 ity of nsp1beta to suppress interferon beta (IFN-beta) activation and also impaired nsp1beta's functi

65 ntagonizes the induction of interferon beta (IFN-beta) by interacting with and degrading retinoic aci

66 cellular pretreatment with interferon beta (IFN-beta) in a dose-dependent manner.

67 sensitive to inhibition by interferon beta (IFN-beta) in vitro and functions as a highly efficacious

68 show that lack of cytokine interferon-beta (IFN-beta) signaling causes spontaneous neurodegeneration

69 ed a significant inverse correlation between IFN-beta and IFN-gamma programs across all conditions.

70 Moreover, both IFN-beta-dependent cis-presentation of IL-15 on NK cells

71 eplication is significantly less affected by IFN-beta in PML(-/-) cells than in parental PML(+/+) cel

72 on of the transcriptional suppressor CREM by IFN-beta and consequent recruitment of histone deacetyla

73 bial peptides was killed more efficiently by IFN-beta than was the wild-type S. aureus, and immunoblo

74 on, sensitivity to mutagen, or inhibition by IFN-beta compared to WT MHV.

75 Here we show that BST-2 upregulation by IFN-beta and interleukin-27 (IL-27) also increases the s

76 bdomain-3 that is differentially utilized by IFN-beta and IFN-alpha for signal transduction.

77 demonstrate that in mouse and human T cells, IFN-beta specifically inhibits the production of IL-2 up

78 c vaccination required all three components, IFN-beta, NAg, and Alum, for inhibition of experimental

79 Sendai virus infection efficiency, decreased IFN-beta, IFN-lambda1, and interferon-stimulated chemoki

80 nally, we report that RIPK1 kinase-dependent IFN-beta production may be elicited in an analogous fash

81 membrane potential regulates STING-dependent IFN-beta induction independently of ATP synthesis.

82 gregates facilitate canonical TRIF-dependent IFN-beta production downstream of the LPS receptor TLR4.

83 s and pathologic tissue injury, in directing IFN-beta production in macrophages.

84 how that catalytic activity of RIPK1 directs IFN-beta synthesis induced by LPS in mice.

85 nctions of viral double-stranded RNA (dsRNA) IFN-beta induction.

86 elevance of increased B cell activity during IFN-beta treatment is unclear.

87 Endogenous IFN-beta has an important role in immune surveillance an

88 irf1 expression does not involve endogenous IFN-beta, STAT1, or STAT2, and inhibition of IL-27 does

89 pression patterns associated with endogenous IFN-beta.

90 ient to impair ERK1/2 activation and enhance IFN-beta expression.

91 In mice, the production of epidermal IFN-beta by LL37 required MAVS, and human wounded and/or

92 an wild-type MHV to restriction by exogenous IFN-beta and that viruses produced in the presence of an

93 ease of HRV, which is prevented by exogenous IFN-beta treatment.

94 augmentation of these responses by exogenous IFN-beta, but not IFN-lambda, protected MCs against HRV

95 When added exogenously, IFN-beta was significantly more effective at protecting

96 3 (IRF3), a transcription factor central for IFN-beta and IFN-stimulated gene expression.

97 that mAb blockade revealed a unique role for IFN-beta in Lyme arthritis development in B6.C3-Bbaa1 mi

98 These results indicate a protective role for IFN-beta in neuronal homeostasis and validate Ifnb mutan

99 we report a positive translational role for IFN-beta, as gene expression profiling of patient-derive

100 However, ExoN(-) virus generated from IFN-beta-pretreated cells had reduced specific infectivi

101 nefit clinically or histopathologically from IFN-beta treatment.

102 at, in addition to known cytokine functions, IFN-beta is antimicrobial.

103 Furthermore, IFN-beta-producing pDCs exhibit enhanced CCR7-dependent

104 Higher IFN-beta levels in vivo increase GBS killing by the host

105 otein, or caspase-1 produced markedly higher IFN-beta in response to DNA.

106 The NleB effector limited host IFN-beta production by inhibiting Lys(63)-linked ubiquit

107 latform further improved induction of type I IFN-beta and activation of innate and adaptive immune ce

108 pression, and type I IFN by measuring IFNB1 (IFN-beta) and CXCL10 expression in human cell lines and

109 l-based assays to investigate this important IFN-beta binding interface that is centered on IFNAR1 re

110 ExoN(-) virus replication did not result in IFN-beta gene expression, and in the presence of an IFN-

111 in human monocytes corroborated its role in IFN-beta regulation.

112 ns respond by producing cytokines, including IFN-beta.

113 or tolerogenic vaccination that incorporates IFN-beta and neuroantigen (NAg) in the Alum adjuvant.

114 and suggest that, in its absence, increased IFN-beta signaling may result in increased neuroinflamma

115 umulation outside the bacteria and increased IFN-beta production.

116 cytogenes infection as a result of increased IFN-beta-mediated apoptosis of major leukocyte cell popu

117 on of each strain in the liver and increases IFN-beta expression in macrophages in culture.

118 d NOD2 knocked-down cells MDP did not induce IFN-beta, irrespective of MOI.

119 the resulting proteins are unable to induce IFN-beta, are intrinsically less stable than wild-type I

120 al dose of poly A:U was sufficient to induce IFN-beta, readily visualized in vivo.

121 P (NOD1 agonist) suppressed HCMV and induced IFN-beta.

122 he dynamic expression of poly(dA:dT)-induced IFN-beta and cGAS transcripts, we have found that induct

123 ed the role of TLR2 and IRAK-1 in RV-induced IFN-beta, IFN-lambda1, and CXCL-10, which require signal

124 how that Group B Streptococcus (GBS) induces IFN-beta production almost exclusively through cGAS-STIN

125 - and TIR-domain containing adapter inducing IFN beta (TRIF) double deficient NOD mice developed the

126 oll-IL-1R domain-containing adapter inducing IFN-beta (TRIF)-dependent cytokine genes in response to

127 oll/IL-1R domain-containing adapter inducing IFN-beta and downstream production of type I IFN were no

128 oll/IL-1R domain-containing adapter inducing IFN-beta-IFN regulatory factor 3 pathway is required for

129 - and TIR-domain-containing adapter-inducing IFN-beta (TRIF)-mediated signaling pathways.

130 receptor domain-containing adapter-inducing IFN-beta and responded poorly to TLR agonists.

131 receptor domain-containing adaptor inducing IFN-beta (TRIF)-dependent signaling pathway leading to I

132 tor (TIR) domain-containing adaptor inducing IFN-beta (TRIF)-dependent signaling.

133 (TLR3-TIR domain-containing adaptor inducing IFN-beta [TRIF] responsive), C/EBPbeta (TLR7-MyD88 respo

134 TRIF (TIR domain-containing adaptor inducing IFN-beta) mediate the recruitment of IRF-3 through a con

135 oll/IL-1R domain-containing adaptor inducing IFN-beta-dependent pathways.

136 oll/IL-1R domain-containing adaptor inducing IFN-beta/ TNFR-associated factor 3 pathway was highly up

137 tivity affects both MyD88- and TRIF-inducing IFN-beta-mediated signaling pathways upstream of IkappaB

138 Instead, MSK1 and -2 inhibit IFN-beta expression via the induction of dual-specificit

139 teria colonization in the airways, inhibited IFN-beta and in the absence of Staphylococcus (S.) aureu

140 The vIRF1-expressing cells also inhibited IFN-beta production following infection with DNA pathoge

141 antiviral responses by assessing interferon (IFN-beta and IFN-lambda1) induction following rhinovirus

142 apoptotic signaling induced beta interferon (IFN-beta) expression and correlatively inhibited B cell

143 e or paracrine signaling by beta interferon (IFN-beta) is essential for many of the responses of macr

144 bited the activation of the beta interferon (IFN-beta) promoter.

145 While there is 1 beta interferon (IFN-beta) protein, there are 12 different IFN-alpha subt

146 n of activation of IRF3 and beta interferon (IFN-beta) transcription.

147 Beta interferon (IFN-beta) transcripts were induced early during A2 or A2

148 IL-1beta), IL-6, IL-10, and beta interferon (IFN-beta).

149 CD95-induced type I interferon (IFN-beta) contributes to the inhibition of gammaherpesvi

150 IRF3 and disrupts IRF3 interaction with its IFN-beta promoter and its coactivator protein (CREB-bind

151 KC IFN-beta production depended on stimulation of mitochond

152 obacterium africanum strain that induces low IFN-beta levels.

153 evels in sepsis patients correlated with low IFN-beta expression, and p21 knockdown in human monocyte

154 ZBP1-mediated cell death via the RIG-I-MAVS-IFN-beta signaling axis.

155 cells were also defective for TRIF-mediated IFN-beta production in response to E. coli infection.

156 An established MS medication, IFN-beta, also diminished EMMPRIN levels on human cells

157 the mechanisms by which C3a and C5a modulate IFN-beta expression during L. monocytogenes infection we

158 ssed higher levels of IFI16 and induced more IFN-beta upon HSV-2 infection.

159 HP1 and HeLa cells causes significantly more IFN-beta production in response to cytosolic nucleic aci

160 ce infected i.v. produced significantly more IFN-beta than did those infected by the foodborne route.

161 Cells expressing NS3/4A and TLR3/MyD88/IFN-beta promoter stimulator 1(-/-) mouse embryonic fibr

162 el link between C. parapsilosis, TLR7, NOD2, IFN-beta, and IL-27, and we have identified an important

163 Blockade of IFN-alpha but not IFN-beta signaling using either an antibody or a selecti

164 ucing ISG transcription, IFN-lambda (but not IFN-beta) specifically activated a translation-independe

165 contributes significantly to the affinity of IFN-beta for IFNAR1, its ability to activate STAT1, the

166 These distinctive characteristics of IFN-beta-producing pDCs are independent of the type I IF

167 omains and residues enabling complexation of IFN-beta to IFNAR1.

168 DC mice showed lower serum concentrations of IFN-beta and IL-12p40, but normal IFN-alpha levels durin

169 Genetic control of IFN-beta expression was also identified in bone marrow-d

170 tivity eliminates the suppressive effects of IFN-beta on IL-2 production.

171 repression was independent of the effects of IFN-beta on ST-induced macrophage cell death, but signif

172 pheral blood (PB) T cells and the effects of IFN-beta were characterized in samples of untreated and

173 acts as an effector of antiviral effects of IFN-beta.

174 IV showed that BBI induced the expression of IFN-beta and multiple IFN stimulated genes (ISGs), inclu

175 monstrate here that macrophage expression of IFN-beta is negatively regulated by mitogen- and stress-

176 We report that B cell expression of IFN-beta is required for optimal survival and TLR7 respo

177 ls of viral growth and greater expression of IFN-beta mRNA in their lungs than mice infected with Cal

178 se data suggest that T1 B cell expression of IFN-beta plays a key role in regulating responsiveness t

179 popolysaccharide (LPS)-induced expression of IFN-beta was elevated in both MSK1/2 knockout mice and m

180 infection of LAD2 MCs induced expression of IFN-beta, IFN-lambda and IFN-stimulated genes.

181 Here we investigate the expression of IFN-beta, IFN-lambda1 (IL-29), IFN-lambda2/3 (IL-28A/B)

182 We observed increased expression of IFN-beta, IFN-lambda1/IL-29, OAS and viperin in asthmati

183 sphorylation of TBK1, IRF3 and expression of IFN-beta.

184 he C and N termini of the B and C helices of IFN-beta, respectively.

185 factor 3 (IRF3) activation and induction of IFN-beta and -alpha4.

186 RF5 signaling was necessary for induction of IFN-beta and IL-12 by S. aureus, and it also contributed

187 on but instead can suppress the induction of IFN-beta in human primary monocytes and monocyte-derived

188 transcripts, we have found that induction of IFN-beta is earlier than cGAS.

189 ifically required for efficient induction of IFN-beta transcription and of numerous ISGs, acting at t

190 stimulation of TLR4, the rapid induction of IFN-beta was inhibited in cells loaded with oxLDL, where

191 The inhibition of IFN-beta pathway by the neutralization antibody to type

192 at several AMDs were effective inhibitors of IFN-beta production and that they functioned by inhibiti

193 The interaction of IFN-beta with its receptor IFNAR1 (interferon alpha/beta

194 a receptor blocking antibody or knockdown of IFN-beta significantly attenuated the inhibitory effect

195 mutations are responsible for low levels of IFN-beta caused by failure of MOLF STING to translocate

196 , also produced TNF-alpha (and low levels of IFN-beta).

197 factor (IRF) pathway with enhanced levels of IFN-beta, elicits increased macrophage autophagy, and ex

198 high SASSAD scores with the lowest levels of IFN-beta, IL-1, and epithelial cytokines.

199 beta expression, as well as the magnitude of IFN-beta cytokine production following activation of inn

200 indings also reveal a potential mechanism of IFN-beta therapy, namely suppression of GM-CSF productio

201 , and reflect on the molecular mechanisms of IFN-beta's immunosuppressive effects through modulation

202 Overexpression of IFN-beta in the CNS of adult wild-type mice, but not of

203 transcription factors, and overexpression of IFN-beta mRNA and protein were similar in MSK1/2 and DUS

204 philic, asthmatics display overexpression of IFN-beta, IFN-lambda1/IL-29 and ISGs in their sputum cel

205 sms were implicated in the overexpression of IFN-beta: first, JNK-mediated activation of c-jun, which

206 To determine whether specific parts of IFN-beta are antimicrobial, we synthesized IFN-beta heli

207 RIPK1 and RIPK3 kinases in the production of IFN-beta during the host inflammatory responses to bacte

208 SV infection induced increased production of IFN-beta in resistant HNSCC cells.

209 IFN, illustrating that de novo production of IFN-beta in response to VSV plays a key role in antivira

210 tionally, we show that optimal production of IFN-beta triggered by poly (dA:dT) or HSV-1 requires IFN

211 1/IFN regulatory factor 3 and production of IFN-beta.

212 i-viral and anti-proliferative properties of IFN-beta.

213 phosphorylation of IRF3, a key regulator of IFN-beta.

214 ngs show that KCs are an important source of IFN-beta and MAVS is critical to this function, and demo

215 These cells are also the major source of IFN-beta, which is significantly induced by S. pyogenes

216 ere an important, but not the only source of IFN-beta.

217 I IFNs, cell populations that are sources of IFN-beta in the tumor microenvironment, and other host r

218 acking NS4 results in increased synthesis of IFN-beta and upregulation of interferon-stimulated genes

219 IPK1 and RIPK3 kinase-dependent synthesis of IFN-beta is markedly induced by avirulent strains of Gra

220 Despite widespread use of IFN-beta, the therapeutic mechanism is still partially u

221 findings add new perspectives to the use of IFN-beta-inducing compounds in tumor therapy.

222 The human type I IFNs include one IFN-beta and multiple IFN-alpha subtypes that share the

223 The crucial role that endogenously produced IFN-beta plays in eliciting an immune response against c

224 that only few pDCs are capable of producing IFN-beta after virus infection or CpG stimulation.

225 Administration of intranasal recombinant IFN beta (10(4) units) with fluticasone and rhinovirus 1

226 Recombinant IFN-beta promoted neurite growth and branching, autophag

227 ontribute to the ability of MSKs to regulate IFN-beta expression.

228 ing AMPK activity also failed to up-regulate IFN-beta and TNF-alpha after treatment with DMXAA or the

229 n patients presenting with an FCDE, early sc IFN beta-1a tiw administration versus DT prolonged time

230 ntense lesion volume change was lower for sc IFN beta-1a tiw versus DT (nominal p<0.01).

231 ensION): patients initially randomised to sc IFN beta-1a and not reaching clinically definite MS (cli

232 uggest that higher cumulative exposure to sc IFN beta-1a may be associated with better clinical outco

233 nd T1 hypointense lesions were lower with sc IFN beta-1a qw (nominal p<0.05) and tiw versus DT (nomin

234 Serum IFN-beta levels from PP2ACalpha-knockout mice treated wi

235 icant contributor to the expression of serum IFN-beta, whereas MyD88 was not.

236 Rather than disrupting TCR signaling, IFN-beta alters histone modifications in the IL-2 promot

237 Specifically, IFN-beta potently represses ST-dependent innate inductio

238 bacterial and fungal beta-glucans stimulate IFN-beta production by dendritic cells (DCs) following d

239 or via nucleofection, selectively stimulates IFN-beta with low IL-8 costimulation.

240 Moreover, C5a and C3a suppress IFN-beta production by acting through their respective r

241 C5a and C3a suppress IFN-beta production in a manner that is dependent on Bru

242 rt in this article that C5a and C3a suppress IFN-beta production in response to L. monocytogenes via

243 g through their specific receptors, suppress IFN-beta expression by modulation of a distinct innate c

244 ies and demonstrated the ability to suppress IFN-beta expression.

245 ouse embryonic fibroblasts (MEFs) suppressed IFN-beta and TNF-alpha induction following stimulation w

246 f IFN-beta are antimicrobial, we synthesized IFN-beta helix 4 and found that it is sufficient to perm

247 Finally, we demonstrate that IFN-beta therapy requires immune-regulatory B cells by s

248 We demonstrated that IFN-beta induces dose-dependent secretion of ISG chemoki

249 Furthermore, we found that IFN-beta increases autoantibody production, implicating

250 We found that IFN-beta was abundantly produced by epidermal keratinocy

251 s were executed through IFN-beta, given that IFN-beta KD reduced the inhibitory effect of Tri-DAP on

252 Overall, this study indicates that IFN-beta + NAg in Alum vaccination elicits NAg-specific,

253 antimicrobial peptides, and we observed that IFN-beta can directly kill Staphylococcus aureus Further

254 The earlier report that IFN-beta is significantly more effective in blocking vir

255 Our data revealed that IFN-beta is induced by C. parapsilosis, which in turn si

256 of human or murine macrophages reveals that IFN-beta selectively restricts the transcriptional respo

257 We show that IFN-beta(-/-) mice exhibit greater resistance to oral ST

258 Further analysis showed that IFN-beta alone or synergizing with CD95 blocked the acti

259 pe S. aureus, and immunoblotting showed that IFN-beta interacts with the bacterial cell surface.

260 The IFN-beta overproduction observed in the absence of CdnP

261 sions suggested a link between IL-27 and the IFN-beta induced IL-10 pathway.

262 Certain cytokines appear to augment the IFN-beta response through the NF-kappaB pathway.

263 Parts of the IFN-beta molecular surface (especially helix 4) are cati

264 ignificantly inhibited the activation of the IFN-beta promoter after Sendai virus infection or poly(I

265 NS1 also suppressed the activation of the IFN-beta promoter when it was stimulated by interferon r

266 th C5a and C3a reduced the expression of the IFN-beta signaling molecules DDX41, STING, phosphorylate

267 Guided by the crystal structure of the IFN-beta-IFNAR1 complex, we used truncation variants and

268 ytomegalovirus immediate-early promoter, the IFN-beta promoter, and a promoter containing interferon-

269 aprolin, which we show is able to target the IFN-beta mRNA.

270 ficient binding of IRF3/CBP complexes to the IFN-beta promoter in the context of infection.

271 ated activation of c-jun, which binds to the IFN-beta promoter, and second, p38-mediated inactivation

272 g complex, the key residues underpinning the IFN-beta-IFNAR1 interaction are unknown.

273 In this work, we have in vivo visualized the IFN-beta required for the antitumor immune response elic

274 IFNbeta/YFP reporter mice, we identify these IFN-beta-producing cells in the spleen as a CCR9(+)CD9(-

275 This IFN-beta-mediated transcriptional repression was indepen

276 NOD1 activities were executed through IFN-beta, given that IFN-beta KD reduced the inhibitory

277 Thus, IFN-beta has the activity spectrum that drives selective

278 sensitivity of parental SP100(+/+) cells to IFN-beta and support replication of the DeltaICP0 virus.

279 TLR2 by lipoproteins does not contribute to IFN-beta production but instead can suppress the inducti

280 ND10 structures increase in cells exposed to IFN-beta.

281 ND10 structures increase in cells exposed to IFN-beta.

282 atory factor 3) signaling cascade leading to IFN-beta production and then promoted maturation of dend

283 ment, and myostatin expression was linked to IFN-beta production.

284 Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFNAR1-mediated signaling and biological proces

285 Unlike IFN-beta + NAg in Alum vaccines, vaccination with TGF-be

286 ions for poly(I:C) to selectively upregulate IFN-beta in airway epithelial cells without a concomitan

287 xerts anti-HCMV activities predominantly via IFN-beta.

288 In vitro IFN-beta + MOG-induced Tregs inhibited EAE when transfer

289 findings provide a molecular basis by which IFN-beta limits T cell responses.

290 diminished following treatment of cells with IFN-beta, and nsp14 G332A genomes were translated less e

291 was inhibited, changes that correlated with IFN-beta expression.

292 ctivation of this pathway is correlated with IFN-beta production and induction of antitumor T cells.

293 idues Tyr(240) and Tyr(274) interacting with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Va

294 ulated following treatment of monocytes with IFN-beta and Mycobacterium leprae, the intracellular bac

295 Treatment of neurons with IFN-beta induced a similar response, and cluster formati

296 plicities of infection (MOI) without or with IFN-beta or IFN-lambda.

297 Combination therapy with IFN-beta-1a (Avonex) and mycophenolate mofetil (Cellcept

298 Treatment with IFN-beta (IFN-beta) led to a less aggressive epithelial/

299 gh levels of U-ISGF3 and that treatment with IFN-beta reduces CSC properties, suggesting a therapeuti

300 Vaccination with IFN-beta + NAg in Alum ameliorated NAg-specific sensitiz