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1 i-inflammatory cytokines (interleukin 10 and interferon-beta).
2 gulate expression of SP100-related genes and interferon beta.
3 gnaling pathway, as determined by endogenous interferon beta.
4 repeated challenge by LPS if pretreated with interferon beta.
5 initial treatment with glatiramer acetate or interferon beta.
6 with the first line multiple sclerosis drug, interferon beta.
7 ve named L2 that regulates the expression of interferon-beta.
8 g to the activation of IRF3 and induction of interferon-beta.
9 e promotes Leishmania donovani infection via interferon-beta.
10 r probabilities of disability improvement as interferon beta (0.98 [0.65-1.49], p=0.93) and fingolimo
11 Treatment of CS-exposed ALI cultures with interferon beta-1 abrogated the viral infection, suggest
12 stratified by site, to receive subcutaneous interferon beta 1a 44 mug, intravenous alemtuzumab 12 mg
14 187 (96%) of 195 patients randomly allocated interferon beta 1a and 376 (97%) of 386 patients randoml
15 202 (87%) of 231 patients randomly allocated interferon beta 1a and 426 (98%) of 436 patients randoml
21 plan-Meier estimates, 59% of patients in the interferon beta 1a group were relapse-free at 2 years co
22 mpared with 134 [66%] of 202 patients in the interferon beta 1a group) that were mostly mild-moderate
23 adverse events compared with 12 (6%) in the interferon beta 1a group, and three (1%) had immune thro
26 disability, comparing alemtuzumab 12 mg and interferon beta 1a in all patients who received at least
27 cacy and safety of alemtuzumab compared with interferon beta 1a in patients who have relapsed despite
32 rate was lower with daclizumab HYP than with interferon beta-1a (0.22 vs. 0.39; 45% lower rate with d
33 5% CI 43.2-60.7%) than patients treated with interferon beta-1a (15 of 66 patients, 27.2%, 17.2-41.4%
34 eeks was lower with daclizumab HYP than with interferon beta-1a (4.3 vs. 9.4; 54% lower number of les
35 ompared with 52 of 107 patients treated with interferon beta-1a (42.6%, 32.4-52.4%; hazard ratio [HR]
36 andomly assigned in a 1:1:1 ratio to receive interferon beta-1a (44 mug subcutaneously three times pe
37 gnificantly lower with ocrelizumab than with interferon beta-1a (9.1% vs. 13.6%; hazard ratio, 0.60;
38 se of either 1.25 or 0.5 mg or intramuscular interferon beta-1a (an established therapy for multiple
39 y and comparable safety of fingolimod versus interferon beta-1a (IFN beta-1a) in paediatric-onset mul
40 ertaken to determine whether combined use of interferon beta-1a (IFN) 30 mug intramuscularly weekly a
42 .25, or 5 mg/day), placebo, or intramuscular interferon beta-1a (IFNbeta-1a IM) during the core studi
43 t benefits of fingolimod 0.5 or 1.25 mg over interferon beta-1a (IFNbeta-1a) in patients with relapsi
44 arison, SPMS subjects from the intramuscular interferon beta-1a (IM IFNbeta-1a) IMPACT study were als
47 mdesivir, hydroxychloroquine, lopinavir, and interferon beta-1a - in patients hospitalized with coron
50 eficial effects of alemtuzumab compared with interferon beta-1a across all analysed patient subsets,
51 participants self-administered intramuscular interferon beta-1a as background anti-inflammatory treat
52 ose of 600 mg every 24 weeks or subcutaneous interferon beta-1a at a dose of 44 mug three times weekl
53 that has demonstrated superior efficacy over interferon beta-1a for relapsing-remitting multiple scle
54 nt-emergent adverse events was higher in the interferon beta-1a group (365 [83.0%] of 440 participant
55 mmon in the daclizumab HYP group than in the interferon beta-1a group (in 65% vs. 57% of the patients
60 m the safety and efficacy of ozanimod versus interferon beta-1a in individuals with relapsing multipl
61 zumab reduced disease activity compared with interferon beta-1a in most of the analysed subgroups.
62 nd efficacy of ozanimod versus intramuscular interferon beta-1a in participants with relapsing multip
63 Efficacy of Natalizumab in Combination With Interferon Beta-1a in Patients With Relapsing-Remitting
64 ibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitti
65 se rate was lower with ocrelizumab than with interferon beta-1a in trial 1 (0.16 vs. 0.29; 46% lower
66 n was 0.02 with ocrelizumab versus 0.29 with interferon beta-1a in trial 1 (94% lower number of lesio
67 ment) significantly favored ocrelizumab over interferon beta-1a in trial 2 (0.28 vs. 0.17, P=0.004) b
68 on natalizumab monotherapy >18 months, 6 on interferon beta-1a monotherapy >36 months, and 5 untreat
69 interferon beta-1a, with rate ratios versus interferon beta-1a of 0.62 (95% CI 0.51-0.77; p<0.0001)
71 uced compared with the previous 12 months of interferon beta-1a therapy (p<0.0001 for T2 lesions at b
72 olimod compared with the previous 12 months (interferon beta-1a to 0.5 mg fingolimod [n=167], 0.31 [9
73 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 [
75 tients to assess the effect of a change from interferon beta-1a to fingolimod, and to compare over 24
77 s compared with the group that switched from interferon beta-1a to fingolimod, we recorded lower ARRs
78 tively evaluated the effect of intramuscular interferon beta-1a treatment following the first demyeli
79 enrolled in the Observational Study of Early Interferon beta-1a Treatment in High Risk Subjects after
80 ginally received 30 mug weekly intramuscular interferon beta-1a were randomly reassigned (1:1) to rec
81 umab HYP showed efficacy superior to that of interferon beta-1a with regard to the annualized relapse
82 gned to ozanimod 0.5 mg, and 441 assigned to interferon beta-1a) and 1138 (86.7%) completed 24 months
86 usly at a dose of 150 mg every 4 weeks, with interferon beta-1a, administered intramuscularly at a do
87 ion of disability compared with subcutaneous interferon beta-1a, and the mean expanded disability sta
88 however, in patients who initially received interferon beta-1a, ARR was lower after switching to fin
90 h ozanimod 0.5 mg, and 0.28 (0.23-0.32) with interferon beta-1a, with rate ratios versus interferon b
101 0 mg (rate ratio [RR] of 0.52 [0.41-0.66] vs interferon beta-1a; p<0.0001), and 0.24 (0.19-0.31) for
105 Whether combined treatment with recombinant interferon beta-1b and lopinavir-ritonavir reduces morta
106 ere randomly assigned to receive recombinant interferon beta-1b plus lopinavir-ritonavir (interventio
107 linical trial comparing early versus delayed interferon beta-1b treatment in 465 patients with a CIS.
108 d to evaluate the impact of early vs delayed interferon beta-1b treatment in patients with clinically
110 IL-17F before and early after treatment with interferon beta-1b was not associated with poor response
111 239 randomly selected patients treated with interferon beta-1b, 250 mug, for at least 2 years in the
114 Among patients with MS mainly treated with interferon beta-1b, low 25(OH)D levels early in the dise
115 with HCV, exhibited increased expression of interferon-beta, 2',5'-oligoadenylate synthetase 1, inte
116 levels for interleukin 6 (IL-6) (+379%) and interferon-beta (+29%), which induce IFITM expression; l
117 ients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160
118 igh levels of ISG15, intrinsic or induced by interferon-beta, accelerate DNA replication fork progres
119 Analysis of a sample of recombinant human interferon-beta allowed the assignment of at least 18 gl
120 ium contrast-enhancing lesions compared with interferon beta alone and might reduce multiple sclerosi
123 apy of patients with multiple sclerosis with interferon beta, although high levels of IL-17F greater
124 or Clinical Excellence (NICE) concluded that interferon beta and glatiramer acetate would be cost eff
125 beta and low-dose daclizumab group p=0.002; interferon beta and high-dose daclizumab group p<0.0001)
126 an in the interferon beta and placebo group (interferon beta and low-dose daclizumab group p=0.002; i
127 hages is related to diminished production of interferon beta and may partly explain the involvement o
128 higher in both daclizumab groups than in the interferon beta and placebo group (interferon beta and l
131 TLR3 and TLR7/8, but not other TLRs, induced interferon-beta and interferon-lambda in bronchial epith
133 high cure rates when combined with pegylated interferon-beta and ribavirin and show promising clinica
134 -/-), TIR-domain-containing adapter-inducing interferon-beta (-/-), and wild-type mice with toll-like
136 nce (TIR) domain-containing adapter-inducing interferon beta) and activation of the transcription fac
137 TRIF (TIR-domain-containing adapter-inducing interferon-beta), and affected interferon regulatory fac
138 proinflammatory cytokines interleukin 1beta, interferon beta, and RANTES (regulated on activation of
139 nscriptional induction of interleukin 1beta, interferon beta, and RANTES in ZIKV-infected podocytes a
141 ency did not change in patients treated with interferon beta; and was more depleted after autologous
142 stant to ConA-induced liver damage, and anti-interferon beta antibody mitigated ConA/HSC-induced inju
145 vitro culture of a microglial cell line with Interferon-beta, but not infected red blood cells, resul
147 AdRGD-PG-hIFNbeta vector encoding the human interferon-beta cDNA (hIFNbeta) was used to transduce hu
148 six drugs (remdesivir, lopinavir-ritonavir, interferon beta, corticosteroids, chloroquine and hydrox
149 receptor-domain-containing adapter-inducing interferon-beta-dependant interferon signaling pathways
150 receptor domain-containing adaptor-inducing interferon-beta-dependent chemokine interferon-gamma-ind
151 tor (TIR) domain-containing adapter-inducing interferon-beta-dependent response that also down-regula
152 ecule/TIR domain-containing adapter-inducing interferon-beta-dependent signaling pathways was further
155 ce displayed reduced Cox-2 protein, elevated interferon beta expression and increased caspase-3 activ
156 lic dinucleotide activation of STING induces interferon beta expression to initiate innate immune def
157 to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 yea
158 ceived fingolimod (0.5/1.25 mg), placebo, or interferon beta for the respective study durations.
159 ientations in vitro had different effects on interferon-beta gene transcription when they were co-exp
161 r long-range elements that interact with the interferon-beta gene, a model system for studying induci
162 n of cellular antiviral genes, including the interferon-beta gene, in response to Pattern Recognition
163 use, type, and timing of the following DMTs: interferon beta, glatiramer acetate, fingolimod, nataliz
166 initially treated with glatiramer acetate or interferon beta had a lower hazard of conversion to seco
167 probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0.66 [95% CI 0.36-1.2
168 initial treatment with glatiramer acetate or interferon beta (HR, 0.66; 95% CI, 0.44-0.99; P = .046);
169 reduced the ability of nsp1beta to suppress interferon beta (IFN-beta) activation and also impaired
170 infected with H5N1 viruses, the induction of interferon beta (IFN-beta) and IFN-inducible genes, incl
171 aB heterodimers, which induce genes encoding interferon beta (IFN-beta) and other immune mediators.
172 1 (NS1) of WNV antagonizes the induction of interferon beta (IFN-beta) by interacting with and degra
173 n of signal transduction pathways leading to interferon beta (IFN-beta) gene induction following viru
174 are sensitive to cellular pretreatment with interferon beta (IFN-beta) in a dose-dependent manner.
175 ne (0DeltaNLS) is sensitive to inhibition by interferon beta (IFN-beta) in vitro and functions as a h
176 PRRSV nsp4, a 3C-like protease, antagonizes interferon beta (IFN-beta) production by cleaving the NF
177 , inhibiting virus-induced activation of the interferon beta (IFN-beta) promoter and interferon regul
178 lexes induced significantly higher levels of interferon beta (IFN-beta) than the polymerase complexes
179 f several inflammation biomarkers, including interferon beta (IFN-beta), interleukin-6 (IL-6), interl
180 on CRISPR screen in cells prestimulated with interferon beta (IFN-beta), we identified a small number
183 sential role in controlling the synthesis of interferon-beta (IFN-beta) and is a protein consisting o
184 erferon regulatory factor-1 (IRF1) to induce interferon-beta (IFN-beta) and subsequent autocrine sign
187 ption factors essential in the activation of interferon-beta (IFN-beta) gene in response to viral inf
188 degradation of DDX41 and less production of interferon-beta (IFN-beta) in response to intracellular
192 Oral administration of acetate mediated interferon-beta (IFN-beta) response by increasing expres
194 nes such as interferon-gamma (IFN-gamma) and interferon-beta (IFN-beta), which can suppress excessive
197 re incubated with interferon gamma (IFNG) or interferon beta (IFNB) and exposed to H pylori, includin
198 ic HMGB2 abundance and impaired induction of interferon beta (IFNB1) mRNA, which encodes a critical a
199 was found to be associated with the highest interferon beta (IFNbeta) and IL-33 levels in the nasal
201 with one of three alternative commonly used interferon beta (IFNbeta) disease modifying drugs: Avone
204 ssion of mRNA for TNF-alpha by 2-fold and of interferon beta (IFNbeta) in a PKR-dependent manner.
205 lidomide kills ABC DLBCL cells by augmenting interferon beta (IFNbeta) production, owing to the oncog
206 core in response to rituximab suggested that interferon beta (IFNbeta) was an important mechanistic c
208 s in the tumor and induce local secretion of interferon beta (IFNbeta), which is a pro-inflammatory c
209 the vesicular stomatitis virus (VSV)-murine interferon beta (IFNbeta)-sodium iodide symporter (NIS)
211 onocytes from B27-Tg rats also produced more interferon-beta (IFNbeta), which attenuated the effect o
212 otein 3 (NLRP3) inflammasome-independent and interferon-beta (IFNbeta)-resistant EAE (termed type B E
213 performed a genome-wide association study in interferon-beta (IFNbeta)-treated MS patients followed b
216 been associated with suboptimal response to interferon beta in patients with relapsing-remitting mul
217 lemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting mul
219 dendritic cells to induce interleukin-12 and interferon-beta in the context of both glycolipid presen
222 ckdown of cGAS inhibited IRF3 activation and interferon-beta induction by DNA transfection or DNA vir
223 transcriptase, but not integrase, abrogated interferon-beta induction by the virus, suggesting that
226 we tested our mutants' sensitivity to type I interferon (beta interferon [IFN-beta]) in restrictive c
227 us type 1 (HAstV-1) infection induces type I interferon (beta interferon [IFN-beta]) production in di
228 d to proinflammatory mediators (IL-12/IL-23, interferon beta, interferon gamma, CD40L) and platelet m
229 by inducing production of cytokines such as interferon-beta, interferon-gamma, and stimulating dendr
230 ntibodies directed against interferon-alpha, interferon-beta, interleukin-1alpha (IL-1alpha), IL-12p3
231 TRIF, TIR-domain-containing adapter-inducing interferon-beta; IRAK, IL-1R-associated kinase; TAK1, TG
232 n ConA-induced liver injury directly via the interferon-beta/IRF1 axis, and by modulating properties
234 receptor domain-containing adapter-inducing interferon-beta is necessary to activate innate immunity
235 TRIF (TIR-domain-containing adapter-inducing interferon-beta) is essential for GN, but not systemic a
236 f WT, TIR domain-containing adapter-inducing interferon-beta knockout, and MyD88 adapter-like knockou
237 gh a combination of lopinavir, ritonavir and interferon beta (LPV/RTV-IFNb) is currently being evalua
238 Single-stranded RNA transcripts induced interferon-beta mediated though RIG-I and PKR activation
239 and MAVS in IBs inhibited the expression of interferon beta mRNA 27-fold following Newcastle disease
241 nts with relapsing-remitting MS treated with interferon beta (n = 868) were compared with untreated c
242 large observational study of treatment with interferon beta or glatiramer acetate provide evidence t
243 le sclerosis activity despite treatment with interferon beta or glatiramer acetate, clinicians often
249 res cyclic GMP-AMP synthase (cGAS)-dependent interferon-beta production and gasdermin D-dependent int
250 or-inducing interferon-beta (TRIF)-dependent interferon-beta production is crucial for caspase-11 act
252 at doses that do not induce Trex1 amplifies interferon-beta production, resulting in recruitment and
254 In contrast, TLR7 agonists induced a strong interferon beta response in the CNS but only low levels
257 regimens were well tolerated and stimulated interferon-beta secretion in tumors, induced tumor regre
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.
261 fferentially active regulatory regions after interferon-beta stimulus, finding that using logistic re
265 t EDSS measurement) were as follows: for the interferon beta-treated cohort, 5.1 years (interquartile
268 A multivariable Cox regression model with interferon beta treatment included as a time-varying cov
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.
281 , the TIR-domain-containing adaptor-inducing interferon-beta (TRIF) was a central mediator of the res
282 receptor domain-containing adapter inducing interferon-beta (TRIF), a Toll-like receptor adapter pro
283 t the TIR domain containing adaptor-inducing interferon-beta (TRIF), an adaptor molecule mediating TL
285 ta 1, TIR-domain containing adapter inducing interferon-beta (TRIF), TRIF-related adaptor molecule, i
286 ndent TIR-domain-containing adapter-inducing interferon-beta (TRIF), which function as cellular senso
287 -1R (TIR) domain-containing adapter-inducing interferon-beta (TRIF)-, TRIF-related adaptor molecule (
288 t and TIR-domain-containing adaptor-inducing interferon-beta (TRIF)-dependent interferon-beta product
289 ) and TIR domain-containing adaptor inducing interferon-beta (TRIF)-dependent signaling pathways, ini
290 - and TIR domain-containing adapter-inducing interferon-beta (TRIF)-dependent type I interferon produ
291 TRAM (TIR domain-containing adapter-inducing interferon-beta (TRIF)-related adaptor molecule), TRIF,
295 -treated HSCs showed increased expression of interferon-beta, tumor necrosis factor-alpha, and CXCL1,
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 version was lower when glatiramer acetate or interferon beta was started within 5 years of disease on
300 ependent expression of the antiviral protein interferon beta, whereas PAR2 negatively regulates expre