ライフサイエンスコーパス: IFN-alpha

1 IFN-alpha also boosted neutrophil- and monocyte-mediated

2 IFN-alpha also inhibited nociceptive transmission by red

3 IFN-alpha and systemic corticosteroids, compared with no

4 IFN-alpha impairs insulin-mediated NO production, and al

5 IFN-alpha injection stimulated an acute inflammatory cyt

6 IFN-alpha is actually a family of 12 distinct proteins,

7 IFN-alpha levels were measured in supernatants, and mRNA

8 IFN-alpha prevents Ag-induced arthritis (AIA), and in th

9 IFN-alpha production was inhibited only in cells infecte

10 IFN-alpha promoting antibody (IPA) counters HIV-specific

11 IFN-alpha significantly down-regulated the protein level

12 IFN-alpha significantly impaired NO production in insuli

13 IFN-alpha treatment also increased the enzymatic IDO1 ac

14 IFN-alpha treatment also led to enhanced neutrophil adhe

15 IFN-alpha-induced nuclear localization of activated STAT

16 IFN-alpha-induced signaling was impaired in the patient

17 (PFS) of bevacizumab or interferon alfa-2b (IFN-alpha-2b) added to octreotide among patients with ad

18 Similarly, the levels of Gal-9, Tim-3, IFN-alpha, IFN-beta, IFN-gamma, and IL-10 were all signi

19 sponsive to the ability of exogenously added IFN-alpha to suppress HCV replication.

20 GAS killing assays before, during, and after IFN-alpha therapy.

21 h all 12 subtypes of human interferon alpha (IFN-alpha) bind the same receptor, recent results have d

22 d magnitude of HIV-induced interferon alpha (IFN-alpha) production.

23 the major side effects of interferon alpha (IFN-alpha) treatment, but the molecular mechanism underl

24 not the case for pegylated interferon alpha (IFN-alpha)-induced neutropenia.

25 ety of corticosteroids and interferon-alpha (IFN-alpha) in adults with such conditions.

26 Interferon-alpha (IFN-alpha) is a key mediator of antiviral immune respons

27 hymocytes deficient in the interferon-alpha (IFN-alpha) receptor IFN-alphaR showed reduced expression

28 within a short timeframe, interferon-alpha (IFN-alpha) treatment for chronic hepatitis C virus (HCV)

29 of substantial amounts of interferon-alpha (IFN-alpha).

30 HSCs show lower levels of interferon-alpha (IFN-alpha)/Jak-Stat1-associated gene expression than FL

31 between two stimulating cytokines, IL-15 and IFN-alpha, which, given together, constitute a potent ap

32 showed decreased responsiveness to IL-2 and IFN-alpha treatment.

33 asis associated with chronic hepatitis B and IFN-alpha (IFNalpha) treatment response in CHB patients.

34 t is differentially utilized by IFN-beta and IFN-alpha for signal transduction.

35 over, CVB3 did not induce IFN-alpha/beta and IFN-alpha/beta-stimulated genes in control cardiomyocyte

36 s) was necessary for increased chemokine and IFN-alpha secretion in response to the parasite.

37 OD (P = .0285), and between the control and IFN-alpha groups for the OD (P = .0424) and worse eye (P

38 ve increases in proinflammatory proteins and IFN-alpha in distal airways.

39 infection is conferred in part by STING and IFN-alpha/beta signaling in both bone marrow-derived and

40 phtheria toxin receptor (DTR) transgenic and IFN-alpha receptor 1-deficient mice, as well as purified

41 Neutralizing anti-IFN-alpha or anti-IFN-omega antibodies were present at d

42 ow similar CpG-induced CD86 levels when anti-IFN-alpha/beta receptor Ab is added.

43 omalizumab treatment increases pDC antiviral IFN-alpha responses in inner-city children with asthma.

44 At a functional level, attenuated IFN-alpha production failed to alter Ag-driven T cell pr

45 ed in human cells ectopically expressing bat IFN-alpha and IFN-beta.

46 ment of IFN-alpha-induced depression, before IFN-alpha, and (2) longitudinal gene expression changes

47 gh amounts of type I IFN-alpha and IFN-beta (IFN-alpha/beta) in the serum and were resistant to letha

48 Synergy between IFN-alpha/beta signaling and efficacy of early adaptive

49 studies using a monoclonal antibody to block IFN-alpha/beta receptor (IFNAR) signaling in humanized m

50 g, leading to impaired HCV clearance by both IFN-alpha and IFN-lambda.

51 ostinfection with BVDV or recombinant bovine IFN-alpha or human IL-28B significantly reduced CD4(+) T

52 In the brain, IFN-alpha induced an acute change in striatal microstruc

53 ot Ido1(-/-) mice were protected from AIA by IFN-alpha, and Kyn, the main IDO1 product, also prevente

54 effect of Vpu was shown to be attenuated by IFN-alpha treatment.

55 This was explained by IFN-alpha-induced mast cell release of exosomes, which t

56 nal output induced in a sustained fashion by IFN-alpha in PCs and linked both to intracellular conjug

57 ctivation of regulatory pathways in ILC2s by IFN-alpha.

58 y is type I interferon (IFN), represented by IFN-alpha and IFN-beta.

59 d transplant potential, which was rescued by IFN-alpha treatment.

60 5 after infection, and the levels of CD137, IFN-alpha, IFN-beta, IFN-gamma, IL-4, and IL-10 in the l

61 fection in trans via coculture with CD169(+) IFN-alpha-treated DCs restored infection, suggesting tha

62 Conversely, IFN-alpha receptor-deficient AGMs (Ifnalphar1(-/-)), had

63 In the spinal cord IFN-alpha was primarily expressed by astrocytes.

64 source of TNF-alpha, IL-12p40, and of course IFN-alpha, whereas cDCs are most efficient in MHC and co

65 or B cells with CD40L, anti-IgM, IL-21, CpG, IFN-alpha, IL-6 or BAFF induces miR-155 and decreases PU

66 human, primary pDCs substantially decreases IFN-alpha production after TLR7/9 activation with differ

67 This Ab-dependent IFN-alpha regulation may be an important mechanism by wh

68 ost disease skin and markedly reduced dermal IFN-alpha levels.

69 Our data indicate that patients who develop IFN-alpha-induced depression have an increased biologica

70 Twenty patients (34%) developed IFN-alpha-induced depression.

71 eased neutrophil and monocyte numbers during IFN-alpha therapy.

72 y a family of 12 distinct proteins, and each IFN-alpha subtype has different efficacies toward differ

73 too low to otherwise stimulate an effective IFN-alpha response.

74 Though effective, IFN-alpha induces marked behavioral changes that, when s

75 differences in coreceptor usage efficiency, IFN-alpha sensitivity and viral fitness each alone may n

76 phosphorylation when stimulated with either IFN-alpha or IFN-lambda1.

77 ckout BMDMs, and knockout BMDMs had elevated IFN-alpha/beta production compared with control BMDMs.

78 in naive rats, whereas removal of endogenous IFN-alpha by a neutralizing antibody induced hyperalgesi

79 osed to patient plasma samples or exogeneous IFN-alpha.

80 and artificial stimuli, as well as exogenous IFN-alpha, and was PI3K dependent.

81 Finally, exogenous IFN-alpha did not substantially protect cardiomyocytes a

82 lication with one or more doses of exogenous IFN-alpha or -gamma before or during the first few days

83 The cDC responses to exogenous IFN-alpha that we evaluated required STAT2 activation, i

84 Constitutively expressed IFN-alpha results in the induction of a subset of IFN-st

85 ng at baseline and 4 hours after their first IFN-alpha injection.

86 and human lupus studies revealed a role for IFN-alpha in vascular abnormalities associated with impa

87 s a predictor of or a therapeutic target for IFN-alpha-induced depression.

88 en splenic and intrahepatic lymphocytes from IFN-alpha- and IL-15-treated animals were transferred to

89 of only 10 IFNs, including three functional IFN-alpha loci.

90 and macrophages were required for generating IFN-alpha/beta-induced subsequent protective immunity.

91 us, and within the omalizumab group, greater IFN-alpha increases were associated with fewer exacerbat

92 endocytosis of TLR7/9 ligands to allow high IFN-alpha production.

93 by PapMV in the absence of C3 induced higher IFN-alpha production, resulting in superior immune cell

94 jectives of this study were to determine how IFN-alpha promotes endothelial dysfunction in SLE, focus

95 ting the cognate type I IFN receptor (type I IFN alpha/beta receptor [IFNAR]) to interrupt IFN signal

96 In addition, protein levels of both type I IFN-alpha (P < 0.0001) and beta (P = 0.002) were signifi

97 ficient mice produced high amounts of type I IFN-alpha and IFN-beta (IFN-alpha/beta) in the serum and

98 ller (NK) cells from mice lacking the type I IFN-alpha receptor (Ifnar(-/-)) or STAT1 (which signals

99 ver, significant associations between type I IFN-alpha/beta protein levels with the DNA methylation s

100 that interferons (IFNs), such as type-I IFN (IFN-alpha) and type-II IFN (IFN-gamma) are produced by i

101 Type I IFN (IFN-alpha/beta) and type III IFN (IFN-lambda) function a

102 Type I IFN (IFN-alpha/beta) controls systemic replication, and type

103 Type I IFN (IFN-alpha/beta) is thought to enhance growth of the food

104 Type I IFN (IFN-alpha/beta)-driven immune responses to acute viral i

105 ficient pDCs produce more of the type I IFN, IFN-alpha, in vitro and that Siglec-H knockout (KO) mice

106 Type I IFNs (IFN-alpha/beta) are induced in inflammatory conditions a

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

108 duced a biphasic IL-33 response and impaired IFN-alpha and IFN-lambda production, which in turn incre

109 e receptor 7 hyporesponsiveness and impaired IFN-alpha production.

110 Omalizumab improved IFN-alpha responses to rhinovirus, and within the omaliz

111 Changes in IFN-alpha- and IL-2-stimulated gene expression were meas

112 tudy, we show that mice with deficiencies in IFN-alpha/beta signaling or stimulator of IFN genes (STI

113 n, and compensates for the inherent delay in IFN-alpha production common to HIV infection and other v

114 -pseudotyped HIV-1 particles was enhanced in IFN-alpha-treated THP-1 monocytoid cells, and this enhan

115 FN-alpha, implicate striatal perturbation in IFN-alpha-induced fatigue, and dissociate this from mech

116 Infection of HIV-1 was rescued in IFN-alpha-treated myeloid cells via upregulation of CD16

117 f sortilin with multiple cytokines including IFN-alpha, and sortilin depletion in plasmacytoid dendri

118 regulates pDC antiviral functions, including IFN-alpha production and phenotypic maturation.

119 Type I interferons (IFNs), including IFN-alpha, upregulate an array of IFN-stimulated genes (

120 cytokine responses at age 3 years, including IFN-alpha and IL-10 responses to certain stimulants and

121 Increased IFN-alpha production contributes to the pathogenesis of

122 interfering RNA knockdown of Tim-3 increased IFN-alpha secretion in response to activation.

123 us could be rescued from the MX2-independent IFN-alpha-induced blocks in THP-1 cells by treatment wit

124 at the antiviral efficacy of each individual IFN-alpha subtype should be evaluated against the specif

125 Fc-dependent IgG-HIV complexes induce IFN-alpha rapidly and in high titers in response to HIV

126 ed that T. gondii invaded but did not induce IFN-alpha or TNF-alpha in human pDC.

127 Moreover, CVB3 did not induce IFN-alpha/beta and IFN-alpha/beta-stimulated genes in co

128 for polyinosinic-polycytidylic acid-induced IFN-alpha/beta production and alloimmunization.

129 S1PR4 signaling, thus decreasing TLR-induced IFN-alpha secretion.

130 ross-linking inhibits critical virus-induced IFN-alpha responses of plasmacytoid dendritic cells (pDC

131 ts into the mechanism by which HIV-1 induces IFN-alpha in pDCs and contributes to HIV-1 pathogenesis.

132 -receptor domain-containing adapter-inducing IFN-alpha (TRIF) and nuclear factor kappaB (NF-kappaB) c

133 lar cytokine staining (ICS) in ZIKV-infected IFN-alpha/beta receptor-deficient HLA transgenic mice.

134 Our results implicate the inflammatory IFN-alpha/Jak-Stat pathway in the developmental maturati

135 However, T. gondii inhibited IFN-alpha and TNF-alpha produced in response to HSV and

136 Twenty-three patients initiating IFN-alpha treatment for hepatitis C underwent qMT imagin

137 y, we explore the role of type 1 interferon (IFN-alpha/beta) signaling on virulence and immunogenicit

138 stimulatory properties of alpha interferon (IFN-alpha) and interleukin-15 (IL-15), this study explor

139 Other than ganciclovir and alpha interferon (IFN-alpha) prophylaxis, no KSHV-associated chemotherapy

140 T cells were treated with alpha interferon (IFN-alpha) to induce high levels of BST2 expression.

141 pregulation in response to alpha interferon (IFN-alpha) was shown to increase the susceptibility of H

142 induced the expression of alpha interferon (IFN-alpha), key cytokines, and cell adhesion molecules (

143 paracrine actions of alpha/beta interferon (IFN-alpha/beta) (type I), IFN-gamma (type II), and IFN-l

144 activation of type I alpha/beta interferon (IFN-alpha/beta) in response to viral infection.

145 eceptor signaling and alpha/beta interferon (IFN-alpha/beta) production.

146 Pretreatment with type I interferons (IFN-alpha and IFN-kappa) increased IL-6 production by co

147 Type I interferons (IFN-alpha/beta) and the more recently identified type II

148 eptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid dendritic cells as wel

149 hat Siglec-H knockout (KO) mice produce more IFN-alpha after murine cytomegalovirus (mCMV) infection

150 In pigs infected with nsp1beta mutants, IFN-alpha production was increased in the lungs at early

151 rations of IFN-beta and IL-12p40, but normal IFN-alpha levels during the first days postinfection.

152 ma interferon (IFN-gamma) treatment, but not IFN-alpha, -beta, or -lambda treatment, dramatically dec

153 on changes from baseline to weeks 4 or 24 of IFN-alpha treatment, separately in those who did and did

154 receptor alpha-chain even in the absence of IFN-alpha/beta signaling, suggesting that in vivo, this

155 ther than CypA contribute to the activity of IFN-alpha-induced blocks.

156 ally, spinal (intrathecal) administration of IFN-alpha reduced inflammatory pain and increased pain t

157 n and remaining pDC produce lower amounts of IFN-alpha in response to viral stimulation.

158 Blockade of IFN-alpha but not IFN-beta signaling using either an ant

159 lls upon exposure to a high concentration of IFN-alpha.

160 nses via secretion of huge concentrations of IFN-alpha.

161 rences associated with future development of IFN-alpha-induced depression, before IFN-alpha, and (2)

162 crucial for USP18-mediated downregulation of IFN-alpha/beta signalling.

163 a signaling blocked the protective effect of IFN-alpha against AIA, but only during sensitization and

164 it inhibits the antiproliferative effect of IFN-alpha on latently infected BL cells.

165 ompletely abrogated the protective effect of IFN-alpha.

166 which the potentially deleterious effects of IFN-alpha are prevented during a secondary infection.

167 We investigated the effects of IFN-alpha on the regulation of p11, 5-HTR1b and 5-HTR4 i

168 and suggest that the detrimental effects of IFN-alpha/beta signaling on the innate immune response t

169 ured in supernatants, and mRNA expression of IFN-alpha pathway genes was determined by using quantita

170 sorafenib also inhibited PBMC expression of IFN-alpha- and IL-2-regulated genes and inhibited NK cel

171 Compared with WT, the expression of IFN-alpha-stimulated genes (ISGs) was reduced in number

172 ar translocation of STAT1, and expression of IFN-alpha-stimulated genes critical for CMV immunity.

173 and activation, augmenting the expression of IFN-alpha/beta, chemerin and its receptor ChemR23, p-cof

174 bers of ISGs expressed at 12 h versus 4 h of IFN-alpha exposure in all three IFN-I signaling-deficien

175 However, the impact of IFN-alpha on mediators that induce vasodilation and modu

176 rferon (IFN)-stimulated genes independent of IFN-alpha, -beta, and -gamma production and/or secretion

177 over a probable sex bias in the induction of IFN-alpha/beta in the cornea during HSV-1 infection.

178 The induction of IFN-alpha/beta, as well as of proinflammatory cytokines

179 s in vivo While cell-free HIV-1 infection of IFN-alpha-treated CD4(+) T cells was robustly decreased,

180 henomenon phenocopied in HIV-1 infections of IFN-alpha-treated primary monocyte-derived macrophages (

181 dy (IPA) counters HIV-specific inhibition of IFN-alpha production, and compensates for the inherent d

182 y type I IFN responses because inhibition of IFN-alpha/beta receptor signaling abrogated DENV-induced

183 ee mutated viruses stimulated high levels of IFN-alpha expression and exhibited a reduced ability to

184 low SASSAD scores with the lowest levels of IFN-alpha, tissue inhibitor of metalloproteinases 1, and

185 dendritic cells generated in the presence of IFN-alpha and GM-CSF (IFN-DC) and loaded with apoptotic

186 In conclusion, presence of IFN-alpha at Ag sensitization activates an IDO1/TGF-beta

187 itic cells (pDCs) are the major producers of IFN-alpha, an antiviral cytokine involved in immunomodul

188 role for C3 in regulating the production of IFN-alpha following TLR7 activation.

189 processes resulted in reduced production of IFN-alpha, IFN-gamma, IL-1beta, CCL20, and CCL8, and hig

190 ignificant upregulation in the production of IFN-alpha/beta mRNAs in the lungs.

191 aling for this anti-inflammatory property of IFN-alpha.

192 dendritic cells (pDCs) led to a reduction of IFN-alpha secretion, suggesting a pivotal role of sortil

193 is, as a key transcriptional co-regulator of IFN-alpha/Stat1 signaling.

194 g cells and plasmablasts, via the release of IFN-alpha and CD40 engagement.

195 pecific mechanism accounting for the role of IFN-alpha in immunosuppression and predicts that type I

196 However, little is known about the role of IFN-alpha in regulating pain sensitivity and synaptic tr

197 Blocking of FDC secretion of IFN-alpha restored B cell tolerance and reduced the amou

198 was also shown to influence the secretion of IFN-alpha.

199 e of sortilin in the exocytic trafficking of IFN-alpha in pDCs.

200 15 mg/kg every 21 days or 5 million units of IFN-alpha-2b three times per week.

201 After 4 weeks of IFN-alpha treatment, 592 genes were modulated in the who

202 ly, at baseline and monthly over 24 weeks of IFN-alpha treatment.

203 -infected red blood cells in vitro; but only IFN-alpha and IFN-beta were significantly increased afte

204 that mVP35, like eVP35, suppresses not only IFN-alpha/beta production but also proinflammatory respo

205 or exposed to IFN-gamma/interleukin-1beta or IFN-alpha.

206 nt enrichment of rare variations in TLR3- or IFN-alpha/beta-related genes.

207 e be a promising tool to restrict pathogenic IFN-alpha production.

208 period and correlated with increases in PBMC IFN-alpha responses.

209 icate that omalizumab treatment augments pDC IFN-alpha responses and attenuates pDC FcepsilonRIalpha

210 enza-induced PBMC and rhinovirus-induced pDC IFN-alpha responses in the presence of IgE cross-linking

211 Peg-IFN-alpha up-regulated the expression of DAPK and mTOR,

212 n the era of pegylated interferon-alpha (Peg-IFN-alpha) and ribavirin regimens.

213 plays a role in the pegylated IFN-alpha (peg-IFN-alpha)-induced antiviral activity against hepatitis

214 e used to study the relationship between peg-IFN-alpha and the DAPK-mammalian target of rapamycin (mT

215 f DAPK reduced the expression of mTOR in peg-IFN-alpha-treated cells, whereas silencing of mTOR had n

216 ntly mitigated the inhibitory effects of peg-IFN-alpha on HCV replication.

217 hway is critical for anti-HCV effects of peg-IFN-alpha.

218 ssessed the role of DAPK and mTOR in the peg-IFN-alpha-induced suppression of HCV replication.

219 ential treatment of Entecavior and PEGylated IFN-alpha were recruited.

220 zed inflammatory skin reactions at pegylated IFN-alpha injection sites, were analyzed for the express

221 ronic HCV treated with combination pegylated IFN-alpha, ribavirin, and telaprevir/boceprevir.

222 Skin biopsies obtained from pegylated IFN-alpha-associated exanthemas, as well as from localiz

223 d whether DAPK plays a role in the pegylated IFN-alpha (peg-IFN-alpha)-induced antiviral activity aga

224 ve patients, patients treated with PEGylated IFN-alpha, and patients with sequential treatment of Ent

225 to random assignment (MAP, n = 359; MAP plus IFN-alpha-2b, n = 357), with baseline characteristics ba

226 g IPA has the potential to initiate a potent IFN-alpha response early in the course of HIV mucosal in

227 ry identifies IFN-alpha14 as a more powerful IFN-alpha subtype for use in combination therapy trials

228 expression of IL28B and IL-29 and prevented IFN-alpha antiviral activity in HCV cell culture.

229 s induced basal ISG expression and prevented IFN-alpha antiviral activity.

230 in the whole sample, representing primarily IFN-alpha-responsive genes.

231 sured by their decreased capacity to produce IFN-alpha.

232 frequency of pDCs expressing Tim-3 produced IFN-alpha or TNF-alpha in response to the TLR7 agonists

233 In response to injection of purified IFN-alpha/beta or -lambda, IECs in EW-infected mice exhi

234 Patients were randomly assigned to receive IFN alpha-2b at 20 MU/m(2)/d IV for 5 days (Monday to Fr

235 sfunctional pDCs and may negatively regulate IFN-alpha, possibly through interference with TLR signal

236 ts, whereas expression of WT IFNAR1 restored IFN-alpha-mediated suppression of CMV.

237 (+)CD38(hi) Breg cells conversely restrained IFN-alpha production by pDCs via IL-10 release.

238 Robust IFN-alpha/beta production was abolished when gene encodi

239 Second, IFN-alpha, which has been a mainstay of HBV and HCV ther

240 ced IL-8 and IL-10 while CD1(-) cDC secreted IFN-alpha, IL-12 and TNF-alpha.

241 the genomic loci of Stat1 as well as several IFN-alpha effector genes, acting to regulate their expre

242 Since IFN-alpha acts by different mechanism than ARVs and has

243 We demonstrate that IFN-alpha promotes an endothelial dysfunction signature

244 We found that IFN-alpha and IFN-lambda1 antiviral activity against HCV

245 We found that IFN-alpha signaling is transient and becomes refractory

246 We found that IFN-alpha therapy enhanced GAS killing in whole blood ex

247 Strikingly, we found that IFN-alpha/beta receptor (type-I IFN receptor) was expres

248 We hypothesized that IFN-alpha induces a compensatory innate antibacterial st

249 The results indicated that IFN-alpha treatment resulted in p11 down-regulation, whi

250 We further report that IFN-alpha, in the absence of an adjuvant, is sufficient

251 SLE and other autoimmune diseases affect the IFN-alpha production in healthy individuals.

252 the IFN-gamma receptor (IFN-gammaR) and the IFN-alpha/beta receptor IFNAR1.

253 AR1 (IFNAR1*557Gluext*46), which encodes the IFN-alpha receptor signaling subunit.

254 f the P90A mutant but modestly increased the IFN-alpha sensitivity of wild-type virus.

255 in highly immunocompromised mice lacking the IFN-alpha/beta receptor.

256 Thus, FDCs are a critical source of the IFN-alpha driving autoimmunity in this lupus model.

257 nuclear translocation and inhibition of the IFN-alpha response was partially reversed by a deficienc

258 ponse in NOD DCs is likely downstream of the IFN-alpha/beta receptor because DCs from NOD and B6 mice

259 hat over-expression of p11 could prevent the IFN-alpha-induced down-regulation of 5-HTR1b and 5-HTR4.

260 t after triggering of arthritis, subdued the IFN-alpha-induced inhibition of mBSA-induced proliferati

261 PR)/Cas9 technology, we demonstrate that the IFN-alpha hypersensitivity of these mutants in THP-1 cel

262 apsilosis, which in turn signals through the IFN-alpha/beta receptor and STAT1/2 to induce IL-27.

263 l, we demonstrate that signaling through the IFN-alpha/beta receptor is required for inflammation-ind

264 Furthermore, the three IFN-alpha genes are constitutively expressed in unstimul

265 creasing the apoptosis rate of ILC2s through IFN-alpha production.

266 214 were allocated to bevacizumab and 213 to IFN-alpha-2b.

267 Here we show that in addition to IFN-alpha, IFN-beta and IL-27 also affect Vpu-mediated B

268 udy design to measure acute brain changes to IFN-alpha and relate these to later development of discr

269 Chronic exposure of mice to IFN-alpha alone was sufficient to strongly suppress spec

270 f coreceptor usage efficiency, resistance to IFN-alpha and viral fitness were not associated with pro

271 Resistance to IFN-alpha was also different between T/F viruses in 2 of

272 ased phosphorylation of STAT1 in response to IFN-alpha is associated with detectable activation of ST

273 ction of IFN-stimulated genes in response to IFN-alpha stimulation and it inhibits the antiproliferat

274 , RANTES, MIP1-alpha, and MIG in response to IFN-alpha stimulation.

275 eas signal pathway activation in response to IFN-alpha was rapid and transient in WT MGCs, this was d

276 We thus hypothesized that the responses to IFN-alpha treatment of chronic hepatitis B (CHB) patient

277 ed those who were and were not responsive to IFN-alpha treatment with correct rate of 84.00% and 71.7

278 have an increased biological sensitivity to IFN-alpha, as shown by larger gene expression changes, a

279 p mutation P90A, all increase sensitivity to IFN-alpha-mediated inhibition.

280 ate exquisite sensitivity of the striatum to IFN-alpha, implicate striatal perturbation in IFN-alpha-

281 ily in the epidermis and induced a transient IFN-alpha response.

282 ment, but the molecular mechanism underlying IFN-alpha-induced depression remains unclear.

283 d dissociate this from mechanisms underlying IFN-alpha-induced mood symptoms, providing empirical sup

284 s-presenting to CD8(+) T cells in vitro upon IFN-alpha, CpG, and LPS stimulation, and also in cross-p

285 ur study introduces a novel pathway by which IFN-alpha serves as a proatherogenic mediator through re

286 form of neuronal-glial interaction by which IFN-alpha, produced by astrocytes, inhibits nociceptive

287 Along with IFN-alpha and IFN-beta, IFN-gamma was demonstrated to co

288 f dendritic cell (DC)-T cell cocultures with IFN-alpha upregulated CD169 expression on DCs and rescue

289 erified that potency at TLR7 correlates with IFN-alpha/beta production in human blood, whereas IFN-ga

290 Treatment of AGM HSCs with IFN-alpha enhanced long-term hematopoietic engraftment a

291 We found that intraperitoneal injection with IFN-alpha in Balb/c mice resulted in an increased immobi

292 /-), or Ifnar(-/-) mice, treated or not with IFN-alpha or the IDO1 product kynurenine (Kyn).

293 ngs raise the possibility that patients with IFN-alpha/beta-mediated conditions, including autoimmuni

294 Pretreatment with IFN-alpha failed to suppress CMV protein expression in p

295 et cell stimulation, even after priming with IFN-alpha.

296 Perfusion of spinal cord slices with IFN-alpha suppressed excitatory synaptic transmission by

297 ith hepatitis C virus infection treated with IFN-alpha killed group A Streptococcus (GAS) better than

298 ial immune defenses in patients treated with IFN-alpha.

299 Protective treatment with IFN-alpha increased the expression of IDO1 in pDC during

300 d STAT5 phosphorylation after treatment with IFN-alpha or IL-2.