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1 IFN-alpha and systemic corticosteroids, compared with no
2 IFN-alpha impairs insulin-mediated NO production, and al
3 IFN-alpha increased HLA-DR, CD80, CD86, and PD-L1 expres
4 IFN-alpha levels were measured in supernatants, and mRNA
5 IFN-alpha limits CHIKV replication and dissemination, wh
6 IFN-alpha production was inhibited only in cells infecte
7 IFN-alpha significantly impaired NO production in insuli
8 IFN-alpha significantly increased depression symptoms (H
9 IFN-alpha treatment also led to enhanced neutrophil adhe
10 IFN-alpha-induced signaling was impaired in the patient
11 IFN-alpha-mediated inhibition of IL-12 production, rathe
12 IFN-alpha/-beta have very low basal expression levels bu
13 (PFS) of bevacizumab or interferon alfa-2b (IFN-alpha-2b) added to octreotide among patients with ad
14 apeutic efficacy of the AAV-IFN-alpha or AAV-IFN-alpha fused to apolipoprotein A-1 vectors in experim
15 hylactic and therapeutic efficacy of the AAV-IFN-alpha or AAV-IFN-alpha fused to apolipoprotein A-1 v
18 ated by others and us that interferon alpha (IFN-alpha) treatment of hepatocytes induced a prolonged
22 mycin (mTOR) signaling and interferon-alpha (IFN-alpha) production by plasmacytoid dendritic cells.
23 ver, a prolonged, elevated interferon-alpha (IFN-alpha) response is associated with a negative diseas
24 hird of patients receiving Interferon-alpha (IFN-alpha) treatment for Hepatitis-C develop major depre
25 interferons, particularly interferon-alpha (IFN-alpha), play a vital role in the host's anti-viral d
26 t of myeloid cells that are resistant, in an IFN-alpha/beta-dependent manner, to VEEV-induced macromo
27 ] vs 12.0 pg/ml [12.0, 126.7]; p = .03), and IFN-alpha (5.1 pg/mL [5.1, 5.1] vs 5.1 pg/ml [5.1, 26.3]
30 over, CVB3 did not induce IFN-alpha/beta and IFN-alpha/beta-stimulated genes in control cardiomyocyte
32 OD (P = .0285), and between the control and IFN-alpha groups for the OD (P = .0424) and worse eye (P
36 with strong downregulation of IFN-gamma and IFN-alpha gene signatures that were reversed by treatmen
37 eutralizing antibodies against IFN-gamma and IFN-alpha/beta receptor subunit 1, and their cellular so
41 4815; TT) is associated with spontaneous and IFN-alpha-dependent cure of hepatitis C virus infection.
42 s essential for TLR9-driven suppression, and IFN-alpha cannot compensate for impaired IFN-gamma signa
43 eurons revealed normal responses to TLR3 and IFN-alpha/beta stimulation but abnormal responses to HSV
44 phtheria toxin receptor (DTR) transgenic and IFN-alpha receptor 1-deficient mice, as well as purified
45 omalizumab treatment increases pDC antiviral IFN-alpha responses in inner-city children with asthma.
46 ) and interleukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-beta, and TNF-alpha mRNA levels induced b
51 studies using a monoclonal antibody to block IFN-alpha/beta receptor (IFNAR) signaling in humanized m
52 In support of our a-priori hypothesis, both IFN-alpha and anti-TNF significantly modulated amygdala
53 . aureus was observed after exposure to both IFN-alpha and -gamma, whereas IFN-gamma appeared to inhi
60 fection in trans via coculture with CD169(+) IFN-alpha-treated DCs restored infection, suggesting tha
62 e possibility of exploring such short-course IFN-alpha treatments for the enhancement of effector cel
63 nt experiments were carried out to determine IFN-alpha resistance, replication fitness, and viral pro
66 potential of sustained delivery of low-dose IFN-alpha for the treatment of MS and likely other T cel
70 and fibrosis, which do not depend on either IFN-alpha/beta receptor signaling or mixed lineage kinas
72 ckout BMDMs, and knockout BMDMs had elevated IFN-alpha/beta production compared with control BMDMs.
76 -molecular-weight/LyoVec and LPS to evaluate IFN-alpha and TNF-alpha production capacities (RIG-I and
80 lication with one or more doses of exogenous IFN-alpha or -gamma before or during the first few days
82 bepithelial monocytes/macrophages expressing IFN-alpha/beta in asthmatic patients during infection.
83 blood sampling before and after their first IFN-alpha (4-h) or anti-TNF (24-h) injection and follow-
84 Vs, we developed knockout (KO) HIE lines for IFN alpha and lambda receptors and the signaling molecul
85 IRF3, transcription factor was critical for IFN-alpha/beta induction in vitro and in sera of mice.
87 and human lupus studies revealed a role for IFN-alpha in vascular abnormalities associated with impa
88 Our study uncovers a pathogenic role for IFN-alpha/-beta in facilitating autoimmune toxicity duri
90 oreover, encephalitogenic T lymphocytes from IFN-alpha-treated mice re-exposed to the myelin oligoden
92 IL-13, IL-6, IL-12, interferon (IFN)-gamma, IFN-alpha, IL-2, IL-2 R, IL-8, macrophage inflammatory p
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 ver, significant associations between type I IFN-alpha/beta protein levels with the DNA methylation s
100 duced higher levels of expression of type I (IFN-alpha and IFN-beta) and type III (IFN-lambda1 to IFN
101 ties of the antiviral interferons of type I (IFN-alpha) and type III (IFN-lambda) against SARS-CoV-2
104 e I interferons (IFNs), including alpha IFN (IFN-alpha) and IFN-beta, potently suppress HIV-1 replica
107 YFV NS5 requires the presence of type I IFN (IFN-alpha/beta) for its engagement with human signal tra
110 We sought to understand how type I IFNs (IFN-alpha and IFN-beta) might act directly on nociceptor
114 eving optimal antiviral responses.IMPORTANCE IFN-alpha/beta induction limits CNS viral spread by esta
116 -pseudotyped HIV-1 particles was enhanced in IFN-alpha-treated THP-1 monocytoid cells, and this enhan
117 restored parainfluenza virus 5 infection in IFN-alpha-pretreated, ISG15-deficient cells, confirming
120 P-001 induced cytokine production, including IFN-alpha from plasmacytoid dendritic cells, but only in
121 cytokine responses at age 3 years, including IFN-alpha and IL-10 responses to certain stimulants and
126 novel role for BCAP in promoting TLR-induced IFN-alpha production in pDC and in systemic lupus erythe
129 ross-linking inhibits critical virus-induced IFN-alpha responses of plasmacytoid dendritic cells (pDC
130 -receptor domain-containing adapter-inducing IFN-alpha (TRIF) and nuclear factor kappaB (NF-kappaB) c
131 lar cytokine staining (ICS) in ZIKV-infected IFN-alpha/beta receptor-deficient HLA transgenic mice.
134 ean 48.0 +/- 10.5 years, 21 male) initiating IFN-alpha treatment for Hepatitis-C and 30 (mean 50.4 +/
135 y, we explore the role of type 1 interferon (IFN-alpha/beta) signaling on virulence and immunogenicit
136 quired for the activity of alpha interferon (IFN-alpha) against vesicular stomatitis virus, Indiana s
137 '-deoxyuridine (5BVdU) and alpha interferon (IFN-alpha) and when the antivirals are removed, spontane
138 tested the hypothesis that alpha interferon (IFN-alpha) could improve the function of NK cells from c
139 r chronic hepatitis B, and alpha interferon (IFN-alpha) is the only available immunomodulatory drug,
142 he ability of short-course alpha interferon (IFN-alpha) treatments to effectively enhance such effect
143 pregulation in response to alpha interferon (IFN-alpha) was shown to increase the susceptibility of H
144 induced the expression of alpha interferon (IFN-alpha), key cytokines, and cell adhesion molecules (
145 paracrine actions of alpha/beta interferon (IFN-alpha/beta) (type I), IFN-gamma (type II), and IFN-l
149 eptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid dendritic cells as wel
150 tably, the production of type I interferons (IFN-alpha/beta), IFN-stimulated genes (PKR, OAS, Mx1, an
151 ological analysis revealed that mice lacking IFN-alpha sustained elevated infection in the infected a
154 cccDNA transcription and may partly mediate IFN-alpha silencing of hepadnaviral cccDNA transcription
155 erestingly, blood PDCs secreted 10-fold more IFN-alpha in response to IAV compared with tonsil PDCs.
156 ma interferon (IFN-gamma) treatment, but not IFN-alpha, -beta, or -lambda treatment, dramatically dec
158 , expression of BGLF2 reduced the ability of IFN-alpha to inhibit BZLF1 expression and enhanced EBV r
159 aling; BGLF2 also counteracts the ability of IFN-alpha to suppress EBV reactivation.IMPORTANCE Type I
162 g, a receptor proximal complex consisting of IFN-alpha and -beta receptors 1 and 2 (IFNAR1, IFNAR2, r
163 may partly mediate the suppressive effect of IFN-alpha on hepadnaviral cccDNA transcription.IMPORTANC
166 ured in supernatants, and mRNA expression of IFN-alpha pathway genes was determined by using quantita
167 tochemistry was used to detect expression of IFN-alpha, IFN-beta, and the PRRs: Toll-like receptor 3,
169 ar translocation of STAT1, and expression of IFN-alpha-stimulated genes critical for CMV immunity.
170 anisms underlying the antiviral functions of IFN-alpha in hepadnaviral infection may reveal molecular
171 bers of ISGs expressed at 12 h versus 4 h of IFN-alpha exposure in all three IFN-I signaling-deficien
174 over a probable sex bias in the induction of IFN-alpha/beta in the cornea during HSV-1 infection.
175 s in vivo While cell-free HIV-1 infection of IFN-alpha-treated CD4(+) T cells was robustly decreased,
176 henomenon phenocopied in HIV-1 infections of IFN-alpha-treated primary monocyte-derived macrophages (
177 y type I IFN responses because inhibition of IFN-alpha/beta receptor signaling abrogated DENV-induced
178 mice and that this correlates with a lack of IFN-alpha/beta-induced YFV NS5 ubiquitination in murine
179 low SASSAD scores with the lowest levels of IFN-alpha, tissue inhibitor of metalloproteinases 1, and
180 in secretion of very high systemic levels of IFN-alpha/beta, suggesting that stress responses in resp
183 itic cells (pDCs) are the major producers of IFN-alpha, an antiviral cytokine involved in immunomodul
185 processes resulted in reduced production of IFN-alpha, IFN-gamma, IL-1beta, CCL20, and CCL8, and hig
186 Activation of TLR9 leads to production of IFN-alpha, which drives IFN-gamma production by natural
189 pecific mechanism accounting for the role of IFN-alpha in immunosuppression and predicts that type I
190 this study demonstrated an essential role of IFN-alpha/beta receptor 1 (IFNAR1) specifically in neuro
192 or p22, inhibits the antiviral signaling of IFN-alpha, which sheds light on the enigmatic function o
193 with VEEV to identify the cellular source of IFN-alpha/beta, the timing and extent of translation and
194 mega) (13 patients), against the 13 types of IFN-alpha (36), or against both (52) at the onset of cri
197 B2-mediated steady-state resistive tuning on IFN-alpha induction by pDCs, thereby contributing to SLE
198 eated with an IFN-beta-blocking antibody) or IFN-alpha (IFN regulatory factor 7 knockout [IRF7-KO] mi
203 icate that omalizumab treatment augments pDC IFN-alpha responses and attenuates pDC FcepsilonRIalpha
204 enza-induced PBMC and rhinovirus-induced pDC IFN-alpha responses in the presence of IgE cross-linking
209 al cccDNA transcription.IMPORTANCE Pegylated IFN-alpha is the only therapeutic regimen that can induc
210 ve patients, patients treated with PEGylated IFN-alpha, and patients with sequential treatment of Ent
212 endent fashion in the presence of 5BVdU plus IFN-alpha; and (v) 3D cultures of NPCs are less suscepti
214 frequency of pDCs expressing Tim-3 produced IFN-alpha or TNF-alpha in response to the TLR7 agonists
217 Patients were randomly assigned to receive IFN alpha-2b at 20 MU/m(2)/d IV for 5 days (Monday to Fr
218 IRF3, IRF7, the type I interferon receptor (IFN-alpha and IFN-beta receptor subunit 1 [IFNAR1]), T c
219 ld-type, Scga1b1-Foxo3a-/- mice show reduced IFN-alpha, IFN-beta, IFN-lambda2/3 in response to challe
220 gonucleotides in vitro and in vivo, reducing IFN-alpha secretion and the induction of IFN-stimulated
221 sfunctional pDCs and may negatively regulate IFN-alpha, possibly through interference with TLR signal
225 id cell cultures infected with VEEV secreted IFN-alpha/beta that increased until cell death was obser
226 0) = 220 nM) and >100-fold TLR7 selectivity (IFN-alpha EC(50) > 50 muM) was observed in human periphe
228 (-/-) mice produced significantly less serum IFN-alpha than wild-type mice after injection of TLR9 ag
230 beta expression and numbers of subepithelial IFN-alpha/beta-expressing monocytes/macrophages during i
231 dies demonstrated an association of systemic IFN-alpha/beta production with myeloid cell infection ef
232 ental IFN that appeared less protective than IFN-alpha, suggesting a potential weakness in antiviral
234 nce of our research is in demonstrating that IFN-alpha and IFN-beta both have protective roles during
244 and disrupt complex interactions between the IFN-alpha/beta and IFN-gamma pathways in achieving optim
245 tightly regulated communication between the IFN-alpha/beta and IFN-gamma signaling pathways to optim
247 er, the virus rapidly evolves to exploit the IFN-alpha response for its replication, spread, and path
251 nuclear translocation and inhibition of the IFN-alpha response was partially reversed by a deficienc
252 r7 (-/-) Tlr9 (-/-) double-knockout pDC, the IFN-alpha response to MHV68 was completely abolished.
253 o cccDNA minichromosomes and phenocopied the IFN-alpha-induced posttranslational modifications of ccc
255 feron (IFN-alpha/beta) signaling through the IFN-alpha/beta receptor (IFNAR) is essential to limit vi
256 l, we demonstrate that signaling through the IFN-alpha/beta receptor is required for inflammation-ind
257 ere mediated by direct signaling through the IFN-alpha/beta-receptor (IFNAR), as Ab-mediated blocking
258 rn recognition receptors contributing to the IFN-alpha response to MHV68 in pDC are TLR7 and TLR9, bu
259 nistration of a neutralizing antibody to the IFN-alpha/beta receptor (IFNAR) for 3 d, beginning 30 mi
260 sion patterns of factors associated with the IFN-alpha/beta pathway in different CNS resident cell po
265 NG V154M/wild-type (WT) mice were crossed to IFN-alpha/beta receptor (IFNAR) knockout mice to evaluat
266 eAg(+)) patients respond less effectively to IFN-alpha therapy than do HBeAg-negative (HBeAg(-)) pati
267 nuclear cells from healthy donors exposed to IFN-alpha and chronic hepatitis B (CHB) patients startin
270 ies showed that TF viruses were resistant to IFN-alpha during the very near moment of transmission, b
271 ased phosphorylation of STAT1 in response to IFN-alpha is associated with detectable activation of ST
272 ction of IFN-stimulated genes in response to IFN-alpha stimulation and it inhibits the antiproliferat
273 eas signal pathway activation in response to IFN-alpha was rapid and transient in WT MGCs, this was d
275 We thus hypothesized that the responses to IFN-alpha treatment of chronic hepatitis B (CHB) patient
278 in the CBP response including a shift toward IFN-alpha/IFN-gamma and IL-6/Jak/Signal transducer and a
280 3 days after CHB patients started treatment, IFN-alpha inhibited monocyte cytokine production and T-c
282 HIV controller subjects, and higher ex vivo IFN-alpha-induced NK cytotoxicity after 5 wk of ART+Peg-
285 ur study introduces a novel pathway by which IFN-alpha serves as a proatherogenic mediator through re
287 ent of gastric carcinoma and Raji cells with IFN-alpha blocked BZLF1 expression and EBV reactivation;
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 he IFN subtypes during CHIKV infection, with IFN-alpha limiting early viral replication and dissemina
291 ngs raise the possibility that patients with IFN-alpha/beta-mediated conditions, including autoimmuni
292 uld be induced if cells were pretreated with IFN-alpha for longer times, presumably because of inhibi
296 ificantly modulated amygdala reactivity with IFN-alpha acutely enhancing right amygdala responses to
297 Furthermore, in NK cells stimulated with IFN-alpha, the promoter region of Rsad2 was enriched for
298 sphorylation in response to stimulation with IFN-alpha in healthy control peripheral blood mononuclea
299 STAT1 or pSTAT1 levels in cells treated with IFN-alpha, it blocks the nuclear translocation of pSTAT1
300 viruses in cultures treated with and without IFN-alpha, but the difference was significant in the cas