ライフサイエンスコーパス: interferon-beta

1 i-inflammatory cytokines (interleukin 10 and interferon-beta).

2 gnaling pathway, as determined by endogenous interferon beta.

3 repeated challenge by LPS if pretreated with interferon beta.

4 (MS) who had not responded to treatment with interferon beta.

5 gulate expression of SP100-related genes and interferon beta.

6 ve named L2 that regulates the expression of interferon-beta.

7 g to the activation of IRF3 and induction of interferon-beta.

8 n of STAT3, and secretion of IL-6, IL-10 and interferon-beta.

9 ting in secretion of the antiviral cytokine, interferon-beta.

10 r probabilities of disability improvement as interferon beta (0.98 [0.65-1.49], p=0.93) and fingolimo

11 stratified by site, to receive subcutaneous interferon beta 1a 44 mug, intravenous alemtuzumab 12 mg

12 us alemtuzumab 12 mg per day or subcutaneous interferon beta 1a 44 mug.

13 187 (96%) of 195 patients randomly allocated interferon beta 1a and 376 (97%) of 386 patients randoml

14 202 (87%) of 231 patients randomly allocated interferon beta 1a and 426 (98%) of 436 patients randoml

15 40 (20%) patients in the interferon beta 1a group had sustained accumulation of d

16 20 (11%) of patients in the interferon beta 1a group had sustained accumulation of d

17 75 (40%) patients in the interferon beta 1a group relapsed (122 events) compared

18 104 (51%) patients in the interferon beta 1a group relapsed (201 events) compared

19 94 (47%) patients in the interferon beta 1a group were relapse-free at 2 years co

20 plan-Meier estimates, 59% of patients in the interferon beta 1a group were relapse-free at 2 years co

21 mpared with 134 [66%] of 202 patients in the interferon beta 1a group) that were mostly mild-moderate

22 adverse events compared with 12 (6%) in the interferon beta 1a group, and three (1%) had immune thro

23 e thrombocytopenia compared with none in the interferon beta 1a group.

24 fety of first-line alemtuzumab compared with interferon beta 1a in a phase 3 trial.

25 disability, comparing alemtuzumab 12 mg and interferon beta 1a in all patients who received at least

26 cacy and safety of alemtuzumab compared with interferon beta 1a in patients who have relapsed despite

27 Interferon beta 1a was given three-times per week and al

28 Interferon beta 1a was given three-times per week and al

29 mpared with three (2%) patients treated with interferon beta 1a.

30 uzumab versus 85 (45%) patients treated with interferon beta 1a.

31 rate was lower with daclizumab HYP than with interferon beta-1a (0.22 vs. 0.39; 45% lower rate with d

32 5% CI 43.2-60.7%) than patients treated with interferon beta-1a (15 of 66 patients, 27.2%, 17.2-41.4%

33 eeks was lower with daclizumab HYP than with interferon beta-1a (4.3 vs. 9.4; 54% lower number of les

34 ompared with 52 of 107 patients treated with interferon beta-1a (42.6%, 32.4-52.4%; hazard ratio [HR]

35 andomly assigned in a 1:1:1 ratio to receive interferon beta-1a (44 mug subcutaneously three times pe

36 gnificantly lower with ocrelizumab than with interferon beta-1a (9.1% vs. 13.6%; hazard ratio, 0.60;

37 se of either 1.25 or 0.5 mg or intramuscular interferon beta-1a (an established therapy for multiple

38 ertaken to determine whether combined use of interferon beta-1a (IFN) 30 mug intramuscularly weekly a

39 clerosis (SENTINEL) study, patients received interferon beta-1a (IFN-beta-1a) plus natalizumab 300 mg

40 nal changes in the biopharmaceutical product interferon beta-1a (IFN-beta-1a).

41 monotherapy in AFFIRM or in combination with interferon beta-1a (IFNbeta) in SENTINEL.

42 t benefits of fingolimod 0.5 or 1.25 mg over interferon beta-1a (IFNbeta-1a) in patients with relapsi

43 arison, SPMS subjects from the intramuscular interferon beta-1a (IM IFNbeta-1a) IMPACT study were als

44 eks was 16% with daclizumab HYP and 20% with interferon beta-1a (P=0.16).

45 eficial effects of alemtuzumab compared with interferon beta-1a across all analysed patient subsets,

46 764 patients were randomly assigned: 386 to interferon beta-1a and 378 to glatiramer acetate.

47 Interferon beta-1a and glatiramer acetate are commonly p

48 There was no significant difference between interferon beta-1a and glatiramer acetate in the primary

49 ose of 600 mg every 24 weeks or subcutaneous interferon beta-1a at a dose of 44 mug three times weekl

50 that has demonstrated superior efficacy over interferon beta-1a for relapsing-remitting multiple scle

51 mmon in the daclizumab HYP group than in the interferon beta-1a group (in 65% vs. 57% of the patients

52 ower than expected: 258 patients (126 in the interferon beta-1a group and 132 in the glatiramer aceta

53 lizumab HYP group and in 10% of those in the interferon beta-1a group.

54 cing lesions, although patients treated with interferon beta-1a had significantly fewer gadolinium-en

55 Pegylated interferon beta-1a has shown efficacy in a phase 3 trial

56 and accumulation of disability compared with interferon beta-1a in a phase 2 trial.

57 zumab reduced disease activity compared with interferon beta-1a in most of the analysed subgroups.

58 Efficacy of Natalizumab in Combination with Interferon Beta-1a in Patients with Relapsing Remitting

59 Efficacy of Natalizumab in Combination With Interferon Beta-1a in Patients With Relapsing-Remitting

60 ibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitti

61 se rate was lower with ocrelizumab than with interferon beta-1a in trial 1 (0.16 vs. 0.29; 46% lower

62 n was 0.02 with ocrelizumab versus 0.29 with interferon beta-1a in trial 1 (94% lower number of lesio

63 ment) significantly favored ocrelizumab over interferon beta-1a in trial 2 (0.28 vs. 0.17, P=0.004) b

64 on natalizumab monotherapy >18 months, 6 on interferon beta-1a monotherapy >36 months, and 5 untreat

65 tes of disease activity and progression than interferon beta-1a over a period of 96 weeks.

66 In contrast, those treated with interferon beta-1a steadily accumulated disability.

67 uced compared with the previous 12 months of interferon beta-1a therapy (p<0.0001 for T2 lesions at b

68 re randomised to receive 44 mug subcutaneous interferon beta-1a three times per week or 20 mg subcuta

69 olimod compared with the previous 12 months (interferon beta-1a to 0.5 mg fingolimod [n=167], 0.31 [9

70 s 0.22 [0.15-0.31], in months 13-24 p=0.049; interferon beta-1a to 1.25 mg fingolimod [n=174], 0.29 [

71 Switching from interferon beta-1a to fingolimod led to enhanced efficac

72 tients to assess the effect of a change from interferon beta-1a to fingolimod, and to compare over 24

73 Compared with patients switched from interferon beta-1a to fingolimod, continuous treatment w

74 s compared with the group that switched from interferon beta-1a to fingolimod, we recorded lower ARRs

75 tively evaluated the effect of intramuscular interferon beta-1a treatment following the first demyeli

76 enrolled in the Observational Study of Early Interferon beta-1a Treatment in High Risk Subjects after

77 ginally received 30 mug weekly intramuscular interferon beta-1a were randomly reassigned (1:1) to rec

78 n Relapsing MS Disease) study was to compare interferon beta-1a with glatiramer acetate in patients w

79 umab HYP showed efficacy superior to that of interferon beta-1a with regard to the annualized relapse

80 usly at a dose of 150 mg every 4 weeks, with interferon beta-1a, administered intramuscularly at a do

81 ion of disability compared with subcutaneous interferon beta-1a, and the mean expanded disability sta

82 however, in patients who initially received interferon beta-1a, ARR was lower after switching to fin

83 fingolimod at a dosage of 0.5 or 1.25 mg/d, interferon beta-1a, or placebo.

84 crelizumab and in 0.2% of those treated with interferon beta-1a.

85 bility after treatment with alemtuzumab than interferon beta-1a.

86 relapse rates and MRI outcomes compared with interferon beta-1a.

87 le sclerosis, as compared with intramuscular interferon beta-1a.

88 improved after alemtuzumab but not following interferon beta-1a.

89 crelizumab and in 2.9% of those treated with interferon beta-1a.

90 ng were higher with daclizumab HYP than with interferon beta-1a.

91 rophy in high risk CIS patients treated with interferon beta-1a.

92 We tested whether interferon-beta-1a (IFN-beta-1a), which increases CD73 s

93 linical trial comparing early versus delayed interferon beta-1b treatment in 465 patients with a CIS.

94 d to evaluate the impact of early vs delayed interferon beta-1b treatment in patients with clinically

95 In a patient cohort from the pivotal interferon beta-1b trial, the value of clinical and MRI

96 IL-17F before and early after treatment with interferon beta-1b was not associated with poor response

97 239 randomly selected patients treated with interferon beta-1b, 250 mug, for at least 2 years in the

98 Treatment with interferon beta-1b, 250 mug, for at least 2 years.

99 Among patients with MS treated with interferon beta-1b, higher 25(OH)D levels were associate

100 Among patients with MS mainly treated with interferon beta-1b, low 25(OH)D levels early in the dise

101 with HCV, exhibited increased expression of interferon-beta, 2',5'-oligoadenylate synthetase 1, inte

102 levels for interleukin 6 (IL-6) (+379%) and interferon-beta (+29%), which induce IFITM expression; l

103 ients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160

104 ient mice had 6-fold higher plasma levels of interferon-beta, a key regulator of the type I interfero

105 Analysis of a sample of recombinant human interferon-beta allowed the assignment of at least 18 gl

106 ium contrast-enhancing lesions compared with interferon beta alone and might reduce multiple sclerosi

107 T-cell proliferative response compared with interferon beta alone.

108 is disease activity to a greater extent than interferon beta alone.

109 apy of patients with multiple sclerosis with interferon beta, although high levels of IL-17F greater

110 or Clinical Excellence (NICE) concluded that interferon beta and glatiramer acetate would be cost eff

111 ponsive to immunomodulating therapy, such as interferon beta and glatiramer acetate.

112 y, and 230 were randomly assigned to receive interferon beta and high-dose daclizumab (n=75), interfe

113 and placebo group compared with 1.32 in the interferon beta and high-dose daclizumab group (differen

114 beta and low-dose daclizumab group p=0.002; interferon beta and high-dose daclizumab group p<0.0001)

115 bcutaneous daclizumab 2 mg/kg every 2 weeks (interferon beta and high-dose daclizumab group), daclizu

116 rferon beta and high-dose daclizumab (n=75), interferon beta and low-dose daclizumab (n=78), or inter

117 95% CI 34% to 88%; p=0.004) and 3.58 in the interferon beta and low-dose daclizumab group (25%, -76%

118 an in the interferon beta and placebo group (interferon beta and low-dose daclizumab group p=0.002; i

119 ab group), daclizumab 1 mg/kg every 4 weeks (interferon beta and low-dose daclizumab group), or inter

120 hages is related to diminished production of interferon beta and may partly explain the involvement o

121 eron beta and low-dose daclizumab (n=78), or interferon beta and placebo (n=77).

122 eron beta and low-dose daclizumab group), or interferon beta and placebo for 24 weeks.

123 higher in both daclizumab groups than in the interferon beta and placebo group (interferon beta and l

124 m contrast-enhancing lesions was 4.75 in the interferon beta and placebo group compared with 1.32 in

125 nflammation and elevation of plasma level of interferon-beta and -gamma and interleukin-27.

126 mediated by synergy between small amounts of interferon-beta and canonical TNF-induced signals.

127 Induction of Interferon-beta and Ccl4 by lipoproteins was also partia

128 d resistance to antiproliferative effects of interferon-beta and increased colony forming units follo

129 TLR3 and TLR7/8, but not other TLRs, induced interferon-beta and interferon-lambda in bronchial epith

130 Defective Rhinovirus induced interferon-beta and interferon-lambda production has bee

131 high cure rates when combined with pegylated interferon-beta and ribavirin and show promising clinica

132 -/-), TIR-domain-containing adapter-inducing interferon-beta (-/-), and wild-type mice with toll-like

133 -/-), TIR-domain-containing adapter-inducing interferon-beta (-/-), and wild-type mice.

134 nce (TIR) domain-containing adapter-inducing interferon beta) and activation of the transcription fac

135 TRIF (TIR-domain-containing adapter-inducing interferon-beta), and affected interferon regulatory fac

136 proinflammatory cytokines interleukin 1beta, interferon beta, and RANTES (regulated on activation of

137 nscriptional induction of interleukin 1beta, interferon beta, and RANTES in ZIKV-infected podocytes a

138 Moreover, caspase-4, gasdermin D, interferon-beta, and cGAS levels were elevated in the RP

139 ency did not change in patients treated with interferon beta; and was more depleted after autologous

140 stant to ConA-induced liver damage, and anti-interferon beta antibody mitigated ConA/HSC-induced inju

141 ral analysis, as demonstrated using stressed interferon-beta as an example.

142 All patients were treated with intramuscular interferon-beta as part of the prospective study.

143 vitro culture of a microglial cell line with Interferon-beta, but not infected red blood cells, resul

144 Cytosolic DNA stimulates secretion of interferon-beta by cancer cells following activation of

145 receptor-domain-containing adapter-inducing interferon-beta-dependant interferon signaling pathways

146 receptor domain-containing adaptor-inducing interferon-beta-dependent chemokine interferon-gamma-ind

147 tor (TIR) domain-containing adapter-inducing interferon-beta-dependent response that also down-regula

148 ecule/TIR domain-containing adapter-inducing interferon-beta-dependent signaling pathways was further

149 Assembly of interferon-beta enhanceosome from its individual protein

150 s is one of the main components of the human interferon-beta enhanceosome.

151 ze a composite regulatory element within the interferon-beta enhancer (IFNb).

152 acts specifically with the PRDII site of the interferon-beta enhancer by inserting its DNA-binding se

153 cts more strongly with the PRDIV site of the interferon-beta enhancer, especially in the orientation

154 P-regulated enhancer and the virus-inducible interferon-beta enhancer.

155 e pretreatment of human dendritic cells with interferon-beta enhances their immune response to influe

156 ce displayed reduced Cox-2 protein, elevated interferon beta expression and increased caspase-3 activ

157 ) as being essential for IRF3 activation and interferon beta expression triggered by HCMV, as well as

158 level translates into a 43-fold increase of interferon-beta expression.

159 to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 yea

160 ceived fingolimod (0.5/1.25 mg), placebo, or interferon beta for the respective study durations.

161 ientations in vitro had different effects on interferon-beta gene transcription when they were co-exp

162 r long-range elements that interact with the interferon-beta gene, a model system for studying induci

163 n of cellular antiviral genes, including the interferon-beta gene, in response to Pattern Recognition

164 Natalizumab, no treatment, interferon beta, glatiramer acetate, or fingolimod.

165 emorial Hospital, and despite treatment with interferon beta had had two corticosteroid-treated relap

166 probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0.66 [95% CI 0.36-1.2

167 monocyte/macrophages and for the ability of interferon beta (IFN beta) to inhibit ongoing active HIV

168 reduced the ability of nsp1beta to suppress interferon beta (IFN-beta) activation and also impaired

169 infected with H5N1 viruses, the induction of interferon beta (IFN-beta) and IFN-inducible genes, incl

170 1 (NS1) of WNV antagonizes the induction of interferon beta (IFN-beta) by interacting with and degra

171 n of signal transduction pathways leading to interferon beta (IFN-beta) gene induction following viru

172 are sensitive to cellular pretreatment with interferon beta (IFN-beta) in a dose-dependent manner.

173 ne (0DeltaNLS) is sensitive to inhibition by interferon beta (IFN-beta) in vitro and functions as a h

174 for tumor necrosis factor alpha (TNF-alpha), interferon beta (IFN-beta), interleukin 6 (IL-6), interf

175 enhances their ability to produce IL-27 and interferon beta (IFN-beta).

176 TPL-2 signaling pathway in TLR induction of interferon-beta (IFN-beta) and interleukin-10 (IL-10) in

177 sential role in controlling the synthesis of interferon-beta (IFN-beta) and is a protein consisting o

178 erferon regulatory factor-1 (IRF1) to induce interferon-beta (IFN-beta) and subsequent autocrine sign

179 The induction of interferon-beta (IFN-beta) and/or IFN-lambda1 in respons

180 ts interchromosomal associations between the interferon-beta (IFN-beta) gene enhancer and DNA binding

181 ption factors essential in the activation of interferon-beta (IFN-beta) gene in response to viral inf

182 degradation of DDX41 and less production of interferon-beta (IFN-beta) in response to intracellular

183 The expression of interferon-beta (IFN-beta) in virus-infected HeLa cells

184 Interferon-beta (IFN-beta) is the major treatment for mu

185 ently triggers signaling pathways to promote interferon-beta (IFN-beta) production.

186 We show that lack of cytokine interferon-beta (IFN-beta) signaling causes spontaneous

187 nes such as interferon-gamma (IFN-gamma) and interferon-beta (IFN-beta), which can suppress excessive

188 ichia coli lipopolysaccharide, influenza, or interferon-beta (IFN-beta).

189 NF-kappaB, which promoted the production of interferon-beta (IFN-beta).

190 regulatory factor 3 (IRF3) and production of interferon-beta (IFN-beta).

191 re incubated with interferon gamma (IFNG) or interferon beta (IFNB) and exposed to H pylori, includin

192 Interferon-beta (IFNB1) mRNA shows very large cell-to-ce

193 was found to be associated with the highest interferon beta (IFNbeta) and IL-33 levels in the nasal

194 family, via an autocrine mechanism involving interferon beta (IFNbeta) and IL-6.

195 Although interferon beta (IFNbeta) decreases relapse rate and dis

196 with one of three alternative commonly used interferon beta (IFNbeta) disease modifying drugs: Avone

197 itin ligase Pellino1, which are required for interferon beta (IFNbeta) gene transcription.

198 Interferon beta (IFNbeta) has been reported to play an i

199 ssion of mRNA for TNF-alpha by 2-fold and of interferon beta (IFNbeta) in a PKR-dependent manner.

200 In many cell types, type I interferon beta (IFNbeta) inhibits proliferation and ind

201 lidomide kills ABC DLBCL cells by augmenting interferon beta (IFNbeta) production, owing to the oncog

202 core in response to rituximab suggested that interferon beta (IFNbeta) was an important mechanistic c

203 Conversely, interferon beta (IFNbeta) was associated with decreased

204 the vesicular stomatitis virus (VSV)-murine interferon beta (IFNbeta)-sodium iodide symporter (NIS)

205 A single high dose of interferon-beta (IFNbeta) activates powerful cellular re

206 onocytes from B27-Tg rats also produced more interferon-beta (IFNbeta), which attenuated the effect o

207 otein 3 (NLRP3) inflammasome-independent and interferon-beta (IFNbeta)-resistant EAE (termed type B E

208 performed a genome-wide association study in interferon-beta (IFNbeta)-treated MS patients followed b

209 ing the expression of the antiviral cytokine interferon-beta (IFNbeta).

210 ated kinase implicated in virus induction of interferon-beta (IFNbeta).

211 Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity.

212 lemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting mul

213 been associated with suboptimal response to interferon beta in patients with relapsing-remitting mul

214 ed the transcription factor IRF3 and induced interferon-beta in a STING-dependent manner.

215 dendritic cells to induce interleukin-12 and interferon-beta in the context of both glycolipid presen

216 ed transcription of IFNB1, the gene encoding interferon-beta, in the stimulated cells.

217 c.2465G>A mutation enhanced MDA5 function in interferon beta induction.

218 ckdown of cGAS inhibited IRF3 activation and interferon-beta induction by DNA transfection or DNA vir

219 transcriptase, but not integrase, abrogated interferon-beta induction by the virus, suggesting that

220 Interferon-beta induction occurs during acute simian imm

221 Interferon beta (INFbeta) and glatiramer acetate (GA) ar

222 we tested our mutants' sensitivity to type I interferon (beta interferon [IFN-beta]) in restrictive c

223 us type 1 (HAstV-1) infection induces type I interferon (beta interferon [IFN-beta]) production in di

224 d to proinflammatory mediators (IL-12/IL-23, interferon beta, interferon gamma, CD40L) and platelet m

225 by inducing production of cytokines such as interferon-beta, interferon-gamma, and stimulating dendr

226 ntibodies directed against interferon-alpha, interferon-beta, interleukin-1alpha (IL-1alpha), IL-12p3

227 TRIF, TIR-domain-containing adapter-inducing interferon-beta; IRAK, IL-1R-associated kinase; TAK1, TG

228 n ConA-induced liver injury directly via the interferon-beta/IRF1 axis, and by modulating properties

229 Interferon beta is widely prescribed to treat multiple s

230 Additionally, interferon-beta is capable of acting Tlr13 transcription

231 receptor domain-containing adapter-inducing interferon-beta is necessary to activate innate immunity

232 In contrast, interferon-beta is strongly biased toward SWI/SNF-depend

233 Although interferon-beta is the most popular treatment for multip

234 TRIF (TIR-domain-containing adapter-inducing interferon-beta) is essential for GN, but not systemic a

235 f WT, TIR domain-containing adapter-inducing interferon-beta knockout, and MyD88 adapter-like knockou

236 Single-stranded RNA transcripts induced interferon-beta mediated though RIG-I and PKR activation

237 to TNF and discovered that TNF initiates an interferon-beta-mediated autocrine loop that sustains ex

238 and MAVS in IBs inhibited the expression of interferon beta mRNA 27-fold following Newcastle disease

239 In addition, interferon-beta mRNA is present after activation with LT

240 nts with relapsing-remitting MS treated with interferon beta (n = 868) were compared with untreated c

241 large observational study of treatment with interferon beta or glatiramer acetate provide evidence t

242 le sclerosis activity despite treatment with interferon beta or glatiramer acetate, clinicians often

243 ltiple sclerosis and at least one relapse on interferon beta or glatiramer.

244 VS reduces this response 2-fold and blocking interferon beta or its receptor abrogates it.

245 Patients had received fingolimod, interferon beta, or glatiramer acetate for a minimum of

246 Interferon beta plays an important role in attenuation o

247 induced cytokine production and TRIF-induced interferon beta production.

248 res cyclic GMP-AMP synthase (cGAS)-dependent interferon-beta production and gasdermin D-dependent int

249 TNF-induced interferon-beta production depended on interferon-respon

250 or-inducing interferon-beta (TRIF)-dependent interferon-beta production is crucial for caspase-11 act

251 tion placentas formed foci of infection, and interferon-beta production was prolonged.

252 at doses that do not induce Trex1 amplifies interferon-beta production, resulting in recruitment and

253 inhibits RIG-I stimulated IRF3 activity and interferon-beta production.

254 potent inhibition of RLH- and MAVS-mediated interferon-beta promoter activity and in the disruption

255 -stimulated response element (ISRE), and the interferon-beta promoter, whereas knockdown of TRIS inhi

256 In contrast, TLR7 agonists induced a strong interferon beta response in the CNS but only low levels

257 1]) genomes and induces the inflammasome and interferon beta responses.

258 equivalently sensitive to exogenously added interferon-beta, showed no evidence for differential rec

259 containing 2 (NOD2)-dependent activation of interferon-beta signaling and nuclear factor-kappaB.

260 TRIF (TIR domain-containing adapter-inducing interferon beta) signaling pathways.

261 In response to interferon-beta, the T387A mutant of STAT2 is much more

262 tor 4-TIR-domain-containing adapter-inducing interferon-beta (TLR4-TRIF).

263 Activation of Mertk synergized with interferon-beta to tighten cell junctions and prevent vi

264 t EDSS measurement) were as follows: for the interferon beta-treated cohort, 5.1 years (interquartile

265 Interferon-beta-treated cells expressing wild-type STAT2

266 The main outcome measure was time from interferon beta treatment eligibility (baseline) to a co

267 A multivariable Cox regression model with interferon beta treatment included as a time-varying cov

268 azard of disease progression associated with interferon beta treatment.

269 lapsing multiple sclerosis who are receiving interferon beta treatment.

270 baseline, 6, 12 and 24 months after start of interferon-beta treatment.

271 r-domain-containing adaptor protein inducing interferon beta (TRIF) or myeloid differentiation factor

272 ), or TIR domain-containing adaptor inducing interferon beta (TRIF) signaling or an apoptosis-associa

273 8 and TIR-domain-containing adaptor-inducing interferon beta (TRIF), whereas palmitate-induced cerami

274 PK3), TIR-domain-containing adapter-inducing interferon-beta (TRIF) and Z-DNA-binding protein 1 (ZBP1

275 tor (TIR) domain-containing adapter-inducing interferon-beta (TRIF) but less so for signaling via mye

276 uired TIR-domain-containing adapter-inducing interferon-beta (TRIF) but were independent of myeloid-d

277 yD88)/TIR-domain-containing adapter-inducing interferon-beta (TRIF) double knockout littermates, we d

278 r domain containing adaptor protein inducing interferon-beta (TRIF) is an adaptor associated with TLR

279 ither TIR domain-containing adapter-inducing interferon-beta (TRIF) or MyD88 signal transduction.

280 receptor domain-containing adapter-inducing interferon-beta (Trif) signaling.

281 , the TIR-domain-containing adaptor-inducing interferon-beta (TRIF) was a central mediator of the res

282 ) domain-containing adaptor protein inducing interferon-beta (TRIF) were also used for testing their

283 receptor domain-containing adapter inducing interferon-beta (TRIF), a Toll-like receptor adapter pro

284 t the TIR domain containing adaptor-inducing interferon-beta (TRIF), an adaptor molecule mediating TL

285 receptor domain containing adaptor inducing interferon-beta (TRIF), and TRIF-related adaptor molecul

286 ed by TIR-domain-containing adapter inducing interferon-beta (TRIF), but not by MyD88.

287 ndent TIR-domain-containing adapter-inducing interferon-beta (TRIF), which function as cellular senso

288 -1R (TIR) domain-containing adapter-inducing interferon-beta (TRIF)-, TRIF-related adaptor molecule (

289 t and TIR-domain-containing adaptor-inducing interferon-beta (TRIF)-dependent interferon-beta product

290 ) and TIR domain-containing adaptor inducing interferon-beta (TRIF)-dependent signaling pathways, ini

291 TRAM (TIR domain-containing adapter-inducing interferon-beta (TRIF)-related adaptor molecule), TRIF,

292 ) and TIR-domain-containing adaptor-inducing interferon-beta (TRIF).

293 the adapter TIR-containing adaptor inducing interferon-beta (TRIF).

294 -treated HSCs showed increased expression of interferon-beta, tumor necrosis factor-alpha, and CXCL1,

295 d macaques had significantly lower levels of interferon beta, type 1 interferon-inducible gene myxovi

296 th relapsing-remitting MS, administration of interferon beta was not associated with a reduction in p

297 sease duration, and EDSS score), exposure to interferon beta was not associated with a statistically

298 relapsing multiple sclerosis who were taking interferon beta were randomly assigned to receive add-on

299 ependent expression of the antiviral protein interferon beta, whereas PAR2 negatively regulates expre

300 eceptor 1 domain-containing adapter-inducing interferon beta, which together mediate all TLR MyD88-de

301 , hypercapnia did not down-regulate IL-10 or interferon-beta, which do not require NF-kappaB.