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1 IFN-beta and other IFN-related and neuroinflammatory gen
2 IFN-beta did not induce inflammatory cytokine production
3 IFN-beta essentially modulates the host response against
4 IFN-beta induction did not require live bacteria (i.e.,
5 IFN-beta is a key component of the innate immune respons
6 IFN-beta pretreatment was more effective in protecting a
7 IFN-beta significantly inhibited VZV replication in both
8 IFN-beta treatment of primary astrocytes resulted in bot
9 ety of fingolimod versus interferon beta-1a (IFN beta-1a) in paediatric-onset multiple sclerosis (PoM
13 [IFN]-beta-1a intramuscularly [IM], n = 38; IFN-beta-1a subcutaneously [SC], n = 68; IFN-beta-1b SC,
14 38; IFN-beta-1a subcutaneously [SC], n = 68; IFN-beta-1b SC, n = 41; rituximab, n = 31; tocilizumab,
16 fragment (residues 1 to 349) could activate IFN-beta transcription more robustly than full-length NE
17 STING such as 2',3'-cGAMP and also activated IFN-beta and ISG expression; and (v) UL46 binds to both
18 dition to its well-known signaling activity, IFN-beta may be directly antimicrobial and be part of a
19 ng MSD.Measurements and Main Results: Adding IFN-beta to MDMs, alveolar macrophages, and PBECs prior
21 n virus induction of interferon (IFN)-alpha, IFN-beta and IFN-lambda in bronchial epithelial and bron
22 Here we show that in addition to IFN-alpha, IFN-beta and IL-27 also affect Vpu-mediated BST-2 downre
24 was used to detect expression of IFN-alpha, IFN-beta, and the PRRs: Toll-like receptor 3, melanoma d
25 leukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-beta, and TNF-alpha mRNA levels induced by Sendai vi
26 ga1b1-Foxo3a-/- mice show reduced IFN-alpha, IFN-beta, IFN-lambda2/3 in response to challenge with RV
28 ion of Klebsiella hemolysin gene; TNF-alpha; IFN-beta; nucleotide-binding domain, leucine-rich-contai
30 ogical importance of IFN-Is, discovery of an IFN-beta-inducing microbial molecule represents a potent
31 a gene expression, and in the presence of an IFN-beta-mediated antiviral state, ExoN(-) viral RNA lev
32 ent-derived TNBC tumors demonstrates that an IFN-beta metagene signature correlates with improved pat
33 sults in the activation of astrocytes via an IFN-beta-mediated process and that these astrocytes late
34 t [IFN-beta-KO] mice or mice treated with an IFN-beta-blocking antibody) or IFN-alpha (IFN regulatory
37 a, interferon (IFN) regulatory factor 3, and IFN-beta levels than BCG-wild type (WT) in vitro in muri
39 acrophages have increased Akt activation and IFN-beta production but defects in ERK1/2 and STAT3 acti
40 earch is in demonstrating that IFN-alpha and IFN-beta both have protective roles during acute chikung
42 he type I interferon receptor (IFN-alpha and IFN-beta receptor subunit 1 [IFNAR1]), T cells, and B ce
45 evels of expression of type I (IFN-alpha and IFN-beta) and type III (IFN-lambda1 to IFNlambda3) IFNs
46 to understand how type I IFNs (IFN-alpha and IFN-beta) might act directly on nociceptors in the dorsa
50 (IFNs), including alpha IFN (IFN-alpha) and IFN-beta, potently suppress HIV-1 replication by upregul
51 Type 1 IFNs, including the IFN-alphas and IFN-beta, activate the interferon-alpha/beta receptor (I
52 arly viral replication and dissemination and IFN-beta modulating neutrophil-mediated inflammation.IMP
56 ession of IFN regulatory factor 7 (IRF7) and IFN-beta, as well as increased nuclear exclusion of FOXO
62 tact, despite beta-arrestin 2 activation, as IFN-beta, IFN-gamma, IFN-lambda1, IRF7, TRAIL, and MxA e
63 several type I IFN-associated genes, such as IFN-beta and guanylate-binding proteins (GBPs), are down
64 ked to type I IFN signaling pathway, such as IFN-beta, IFN regulatory factor 1, and guanylate-binding
65 wn host factor-independent pathways to avoid IFN-beta-mediated restriction by altering capsid sequenc
67 CHIKV pathogenesis in mice lacking IFN-beta (IFN-beta knockout [IFN-beta-KO] mice or mice treated wit
70 ntagonizes the induction of interferon beta (IFN-beta) by interacting with and degrading retinoic aci
72 sensitive to inhibition by interferon beta (IFN-beta) in vitro and functions as a highly efficacious
73 -like protease, antagonizes interferon beta (IFN-beta) production by cleaving the NF-kappaB essential
74 s-induced activation of the interferon beta (IFN-beta) promoter and interferon regulatory factor 3 (I
75 nificantly higher levels of interferon beta (IFN-beta) than the polymerase complexes of the 2016-17 o
76 ation biomarkers, including interferon beta (IFN-beta), interleukin-6 (IL-6), interleukin-6 receptor
77 in cells prestimulated with interferon beta (IFN-beta), we identified a small number of factors requi
79 we found that the cytokine interferon-beta (IFN-beta) can induce miR-1 expression in mammalian cells
80 tration of acetate mediated interferon-beta (IFN-beta) response by increasing expression of interfero
81 ng type II IFN-gamma signaling, also blocked IFN-beta responses by inhibiting STAT1/STAT2-mediated tr
82 eplication is significantly less affected by IFN-beta in PML(-/-) cells than in parental PML(+/+) cel
83 bial peptides was killed more efficiently by IFN-beta than was the wild-type S. aureus, and immunoblo
88 d mice expressed higher mRNA levels of CCL2, IFN-beta, IL-10, IL-12p40, TNF-alpha, and MIF than young
92 of house dust mite-sensitized mice to dampen IFN-beta expression and prevent the T(H)1-promoting dend
93 Sendai virus infection efficiency, decreased IFN-beta, IFN-lambda1, and interferon-stimulated chemoki
94 pact model in adult male IFN-beta-deficient (IFN-beta(-/-)) mice and assessed post-traumatic neuroinf
95 nally, we report that RIPK1 kinase-dependent IFN-beta production may be elicited in an analogous fash
98 gregates facilitate canonical TRIF-dependent IFN-beta production downstream of the LPS receptor TLR4.
101 that the dominant signaling cascade driving IFN-beta in macrophages (MPhi) in streptococcal infectio
104 ce, an effect that was reversed by exogenous IFN-beta administration, and Ifnar1(-/-) mice had reduce
106 augmentation of these responses by exogenous IFN-beta, but not IFN-lambda, protected MCs against HRV
108 ations.Objectives: The dynamics of exogenous IFN-beta activity were investigated to inform on future
110 Ifnar1(-/-)) and administration of exogenous IFN-beta were used to study the functional role of type-
112 that mAb blockade revealed a unique role for IFN-beta in Lyme arthritis development in B6.C3-Bbaa1 mi
113 we report a positive translational role for IFN-beta, as gene expression profiling of patient-derive
117 ils in response to stimulation by IFN-gamma, IFN-beta, IFN-lambda, IL-4, IL-13, and IL-10 cytokines t
120 d STAT5 phosphorylation downstream of RIG-I, IFN-beta, and interleukin-4 (IL-4), but not granulocyte-
122 pression, and type I IFN by measuring IFNB1 (IFN-beta) and CXCL10 expression in human cell lines and
124 l-based assays to investigate this important IFN-beta binding interface that is centered on IFNAR1 re
126 itive function impairments were decreased in IFN-beta(-/-) TBI mice compared with their injured WT co
129 tal tissues, and depletion of neutrophils in IFN-beta-KO but not IRF7-KO mice mitigated musculoskelet
130 ExoN(-) virus replication did not result in IFN-beta gene expression, and in the presence of an IFN-
134 and suggest that, in its absence, increased IFN-beta signaling may result in increased neuroinflamma
135 cytogenes infection as a result of increased IFN-beta-mediated apoptosis of major leukocyte cell popu
137 utilizes the host NE-TLR machinery to induce IFN-beta necessary for parasite survival and growth duri
138 ng from EAV or PRRSV nsp4 scission to induce IFN-beta production, we serendipitously found that a NEM
139 the resulting proteins are unable to induce IFN-beta, are intrinsically less stable than wild-type I
140 urine VSV infection model, commensal-induced IFN-beta regulated natural resistance to virus infection
142 es whose products affected viral RNA-induced IFN-beta production and highlighted the complexity of th
143 d that EAV nsp4 also inhibited virus-induced IFN-beta production by targeting NEMO for proteolytic cl
146 8 and TIR domain-containing adapter-inducing IFN-beta, thereby dampening the activation of NF-kappaB
148 oll/IL-1R domain-containing adaptor inducing IFN-beta/ TNFR-associated factor 3 pathway was highly up
149 nce [TIR] domain-containing adaptor-inducing IFN-beta (TRIF), in the control of NiV infection in mice
152 teria colonization in the airways, inhibited IFN-beta and in the absence of Staphylococcus (S.) aureu
153 more relevant production of beta interferon (IFN-beta) and IFN-lambda1 in response to baculovirus inf
155 e or paracrine signaling by beta interferon (IFN-beta) is essential for many of the responses of macr
156 pe, T953, downregulates the beta interferon (IFN-beta) response in vitro in equine endothelial cells
157 se to this, a high level of beta interferon (IFN-beta) was produced during NH/P68 infection; in contr
158 activity cannot counteract beta interferon (IFN-beta)-induced restriction of viral infection, are hi
159 golimod (n=107) or once-weekly intramuscular IFN beta-1a (n=108) in this flexible duration study.
160 ts with moderate or severe ARDS, intravenous IFN-beta-1a administered for 6 days, compared with place
161 eveal antiviral effects of acetate involving IFN-beta in lung epithelial cells and engagement of GPR4
162 cies (ROS) levels are elevated, mTOR and IRF/IFN-beta signaling pathways are enhanced, leading to cel
164 in mice lacking IFN-beta (IFN-beta knockout [IFN-beta-KO] mice or mice treated with an IFN-beta-block
165 evaluated CHIKV pathogenesis in mice lacking IFN-beta (IFN-beta knockout [IFN-beta-KO] mice or mice t
167 -) macrophages displayed significantly lower IFN-beta mRNA than background mice macrophages, and the
168 ntrolled cortical impact model in adult male IFN-beta-deficient (IFN-beta(-/-)) mice and assessed pos
171 lly expressed, ORF8b inhibited IRF3-mediated IFN-beta expression induced by Sendai virus and poly(I:C
172 nic:polycytidylic acid (poly I:C) 30 mug/ml, IFN-beta 10 mug/ml, IFN-gamma 10 mug/ml, or medium contr
173 the mechanisms by which C3a and C5a modulate IFN-beta expression during L. monocytogenes infection we
175 HP1 and HeLa cells causes significantly more IFN-beta production in response to cytosolic nucleic aci
179 ucing ISG transcription, IFN-lambda (but not IFN-beta) specifically activated a translation-independe
180 DA/Q112D virus in the presence or absence of IFN-beta, whereas the G94D/G116R mutations affected reve
181 contributes significantly to the affinity of IFN-beta for IFNAR1, its ability to activate STAT1, the
183 s of type I IFNs have led to the approval of IFN-beta for the treatment of relapsing-remitting MS.
189 monstrate here that macrophage expression of IFN-beta is negatively regulated by mitogen- and stress-
191 se data suggest that T1 B cell expression of IFN-beta plays a key role in regulating responsiveness t
192 popolysaccharide (LPS)-induced expression of IFN-beta was elevated in both MSK1/2 knockout mice and m
196 ls, RelA typically induces the expression of IFN-beta, which restrains viral propagation in neighbori
200 stimulation of TLR4, the rapid induction of IFN-beta was inhibited in cells loaded with oxLDL, where
206 of genetic or pharmacological inhibition of IFN-beta, a key component of type I IFN mechanisms to ad
208 he 2014-15 outbreak induced higher levels of IFN-beta despite relatively minor differences in replica
211 31461630
212 eceive an intravenous injection of 10 mug of IFN-beta-1a (144 patients) or placebo (152 patients) onc
214 transcription factors, and overexpression of IFN-beta mRNA and protein were similar in MSK1/2 and DUS
215 philic, asthmatics display overexpression of IFN-beta, IFN-lambda1/IL-29 and ISGs in their sputum cel
216 sms were implicated in the overexpression of IFN-beta: first, JNK-mediated activation of c-jun, which
218 everse transcription only in the presence of IFN-beta, most consistent with a mechanism of the disrup
219 A/DI RNA-expression stimulated production of IFN-beta and IFN-lambda1 and conditioned media from thes
220 RIPK1 and RIPK3 kinases in the production of IFN-beta during the host inflammatory responses to bacte
221 IFN, illustrating that de novo production of IFN-beta in response to VSV plays a key role in antivira
223 fection lasted for 24 hours after removal of IFN-beta and was maintained albeit reduced up to 1 week
225 expression of HSP70 relieved suppression of IFN-beta expression by ORF8b in an IKKepsilon-dependent
226 IPK1 and RIPK3 kinase-dependent synthesis of IFN-beta is markedly induced by avirulent strains of Gra
227 ent Armenia/07 virus blocks the synthesis of IFN-beta, a key mediator between the innate and adaptive
228 population displayed robust transcription of IFN-beta mRNA, and this did not appear to depend on vira
232 cells, the mNLS variant reduced TNF-alpha or IFN-beta mRNA expression to a similar extent as did WT S
233 IL-13 and monocyte responses to IFN-gamma or IFN-beta emerged as opposing predictors of patient survi
235 -hypersensitive virus can evolve to overcome IFN-beta-mediated blocks targeting the viral capsid, we
236 ge cells and subsequently stimulate a potent IFN-beta response in recipient cells via activation of e
237 r cells accumulate cytosolic DNA and produce IFN-beta in a cGAS-STING-dependent manner, which renders
240 ing AMPK activity also failed to up-regulate IFN-beta and TNF-alpha after treatment with DMXAA or the
241 n patients presenting with an FCDE, early sc IFN beta-1a tiw administration versus DT prolonged time
243 ensION): patients initially randomised to sc IFN beta-1a and not reaching clinically definite MS (cli
244 nd T1 hypointense lesions were lower with sc IFN beta-1a qw (nominal p<0.05) and tiw versus DT (nomin
247 bacterial and fungal beta-glucans stimulate IFN-beta production by dendritic cells (DCs) following d
250 rt in this article that C5a and C3a suppress IFN-beta production in response to L. monocytogenes via
251 g through their specific receptors, suppress IFN-beta expression by modulation of a distinct innate c
252 ouse embryonic fibroblasts (MEFs) suppressed IFN-beta and TNF-alpha induction following stimulation w
253 f IFN-beta are antimicrobial, we synthesized IFN-beta helix 4 and found that it is sufficient to perm
255 ociated polysaccharide A, we determined that IFN-beta expression was induced via TLR4-TRIF signaling.
256 antimicrobial peptides, and we observed that IFN-beta can directly kill Staphylococcus aureus Further
258 pe S. aureus, and immunoblotting showed that IFN-beta interacts with the bacterial cell surface.
262 t difference in 28-day mortality between the IFN-beta-1a vs placebo groups (26.4% vs 23.0%; differenc
264 during the study (41 patients [28.5%] in the IFN-beta-1a group and 33 [21.7%] in the placebo group).
265 days (interquartile range, -1 to 20) in the IFN-beta-1a group and 8.5 days (interquartile range, 0 t
267 ignificantly inhibited the activation of the IFN-beta promoter after Sendai virus infection or poly(I
268 NS1 also suppressed the activation of the IFN-beta promoter when it was stimulated by interferon r
270 ood profiles from tuberculosis patients, the IFN-beta-specific neutrophil signature was reduced in tu
272 ated activation of c-jun, which binds to the IFN-beta promoter, and second, p38-mediated inactivation
276 sensitivity of parental SP100(+/+) cells to IFN-beta and support replication of the DeltaICP0 virus.
282 ession increases RIG-I-mediated signaling to IFN-beta and that RAB1B deletion reduces signaling of th
285 Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFNAR1-mediated signaling and biological proces
289 onsistent control of disease activity versus IFN beta-1a (including treatment-naive and younger patie
290 , p=0.014) were lower with fingolimod versus IFN beta-1a, the latter partially due to accelerated atr
292 AS-STING-IRF3 route in ASFV infection, where IFN-beta production or inhibition was found after infect
293 CHIKV replication and dissemination, whereas IFN-beta protects from CHIKV pathogenesis by limiting in
297 idues Tyr(240) and Tyr(274) interacting with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Va
300 gh levels of U-ISGF3 and that treatment with IFN-beta reduces CSC properties, suggesting a therapeuti