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1 ing the production of IFNlambda4, a type III interferon.
2 chemokines KC and monokine induced by gamma interferon.
3 plex and regulated in part through antiviral interferons.
4 uction of both proinflammatory cytokines and interferons.
5 ts the expression of genes induced by type I interferons.
6 s and the major factors for the induction of interferons, a key component in vertebrate innate immuni
9 RFS) and overall survival (OS) for high-dose interferon alfa (HDI) and ipilimumab at 10 mg/kg (ipi10)
11 had been demonstrated by others and us that interferon alpha (IFN-alpha) treatment of hepatocytes in
13 e both neuronal autoantibodies and levels of interferon alpha, two proposed causative agents in neuro
19 es in patients with COVID-19 showed a strong interferon-alpha response and an overall acute inflammat
20 EBV in low-grade LYG include treatment with interferon-alpha2b, whereas high-grade disease requires
21 0.97), and in 243 of 2050 patients receiving interferon and in 216 of 2050 receiving its control (rat
23 wabs demonstrated that in addition to type-I interferon and interleukin-6-dependent inflammatory resp
24 ogical and biochemical parameters as well as interferon and nucleos(t)ide analogue treatment choice.
26 we identified those treated with a pegylated interferon and ribavirin regimen (PEG/RBV, n = 4764) or
27 response that predominantly involves type I interferons and interferon-related genes, whereas the WT
28 ting the transcriptional induction of type I interferons and other genes that collectively establish
29 generated viruses with inactive versions of interferon antagonist nonstructural protein 1 (nsp1), ns
32 g PEDV with inactive versions of three viral interferon antagonists, nonstructural proteins 1, 15, an
33 suppress EBV reactivation.IMPORTANCE Type I interferons are important for controlling virus infectio
34 actions of R. parkeri with inflammasomes and interferons are similar to those of viruses, which can e
35 id DCs (pDCs), the major producers of type I interferon, are principally recognized as key mediators
36 ) of hepatitis C virus (HCV) screening found interferon-based antiviral therapy associated with incre
38 on CRISPR screen in cells prestimulated with interferon beta (IFN-beta), we identified a small number
39 lic dinucleotide activation of STING induces interferon beta expression to initiate innate immune def
40 six drugs (remdesivir, lopinavir-ritonavir, interferon beta, corticosteroids, chloroquine and hydrox
41 Treatment of CS-exposed ALI cultures with interferon beta-1 abrogated the viral infection, suggest
42 y and comparable safety of fingolimod versus interferon beta-1a (IFN beta-1a) in paediatric-onset mul
43 ta 1, TIR-domain containing adapter inducing interferon-beta (TRIF), TRIF-related adaptor molecule, i
49 long-lasting immune stimulation in terms of interferon expression at the injection site and in drain
50 PARP reduced viral replication and increased interferon expression, suggesting that TiPARP functions
51 ccinated infants had increased production of interferon gamma (IFN-gamma) and monokine induced by gam
52 and evaluated CAR-T cell activation through interferon gamma (IFN-gamma) production and CD107a membr
59 titers and median frequencies of F-specific interferon gamma-secreting T cells also increased substa
64 We also demonstrate a role for the cytokine interferon-gamma (IFNgamma) and the enzyme transglutamin
65 d by high levels of infiltrating T cells and interferon-gamma (IFNgamma) signalling, improves the res
66 reduced secretion of interleukin-2 (IL2) and interferon-gamma (IFNgamma), two factors critical for T
70 -1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17, interferon-gamma and differential T and B cell subset ly
71 icacy and safety of emapalumab (a human anti-interferon-gamma antibody), administered with dexamethas
72 afin improved leptin sensitivity via reduced interferon-gamma expression and induced adipose leptin e
73 hrough the rapid synthesis of a glycosylated interferon-gamma fragment and the chemokine-binding prot
74 ction of higher (p < 0.01) concentrations of interferon-gamma in plasma of low responders compared to
79 AK-STAT, immune deficiency and cross-species interferon-gamma pathways, have advanced our understandi
80 e, spike, and nucleocapsid peptides elicited interferon-gamma production, in 27 (59%), 12 (26%), and
81 investigated feasibility and accuracy of an interferon-gamma release assay (IGRA) for detection of T
83 m levels of tumor necrosis factor -alpha and interferon-gamma were significantly increased in the CSD
85 nd neutralizing) and CD4+ T-cell (expressing interferon-gamma, interleukin-2, and CD40 ligand) respon
86 12 induced sustained intratumoural levels of interferon-gamma, substantially reduced its systemic lev
87 vere disease) and 16 unexposed donors, using interferon-gamma-based assays with peptides spanning SAR
88 D11c(+) macrophage) M1-like polarization and interferon-gamma-expressing T-helper type 1 (Th1) cells
89 inally identified as a receptor expressed on interferon-gamma-producing CD4(+) and CD8(+) T cells.
92 ine monophosphate (cGAMP), an agonist of the interferon gene inducer STING (stimulator of interferon
94 he stimulator of the cyclic GMP-AMP synthase interferon genes (cGAS-STING) innate immune pathway.
95 (DDR), cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway activation, and an
96 ed the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway by using two appro
98 gments and then activating the stimulator of interferon genes (STING) cytosolic DNA-sensing pathway a
101 signaling mediated by the cGAS-stimulator of interferon genes (STING) pathway in patient-derived fibr
106 Hepatitis C virus SVR decreased monocyte interferon genes MX1, IFI27, and CD169 in coinfection an
108 lic DNA sensing adaptor STING (stimulator of interferon genes) play a critical role in vascular infla
110 ough the inhibition of RB1 and stimulator-of-interferon-genes (STING) to propagate cells with a high
112 tivates the host cytosolic DNA sensing STING/interferon I pathway, resulting in enhanced cross-primin
113 ion, mediated by CD8 T cell-intrinsic type I interferon (IFN) and signal transducer and activator of
115 ia, and we have shown previously that type I interferon (IFN) contributes to the pathogenesis of this
120 TLR7-mediated disease, which requires type I interferon (IFN) receptor signaling, TLR9-driven fatalit
121 JUNV and MACV infections stimulate a robust interferon (IFN) response in a retinoic acid-inducible g
123 also increased early infectivity and type I interferon (IFN) responses in mouse bone marrow-derived
126 adults with ARDS have elevated expression of interferon (IFN) stimulated genes (ISGs) associated with
127 halitis in the Western world, and the type I interferon (IFN) system is important for antiviral contr
128 t cells secreted increased amounts of type I interferon (IFN), which could be limited by CGAS or STIN
131 myeloid differentiation primary response 88, interferon (IFN)-gamma, interleukin (IL)1-beta, tumor ne
134 tor transporter protein 4 (RTP4) as a potent interferon (IFN)-inducible inhibitor of human pathogens
136 es of COVID-19 lungs, including emergence of interferon (IFN)-mediated inflammatory responses, loss o
139 x of plasmacytoid dendritic cells (pDCs), an Interferon (IFN)-responsive macrophage population, and a
140 ional modeling to investigate how the type I interferon (IFN)-responsive regulatory network operates
141 s by mammalian reovirus requires both type I interferon (IFN)-signaling and viral replication events
144 response that included high levels of gamma interferon (IFN-gamma) and tumor necrosis factor alpha (
146 g plasmacytoid dendritic cells-(pDCs)-Type I interferon (IFN-I) and acts as autoantigen for pathogeni
147 cytoid dendritic cells (pDCs) produce type I interferon (IFN-I) and are traditionally defined as bein
153 ting capacity through activation of a type I interferon (IFN-I)/STAT1 pathway when caspases are inhib
154 s HSCs in the bone marrow (BM) via a type II interferon (IFN-II) or interleukin-1 (IL1) response, res
158 4; infliximab, n = 101; adalimumab, n = 153; interferon [IFN]-beta-1a intramuscularly [IM], n = 38; I
160 to intracellular dsRNA by expressing type I interferons (IFNs) and inducing apoptosis, but that they
161 s ongoing global threat, type I and type III interferons (IFNs) are currently being evaluated for the
168 of antiviral effectors in response to type I interferons.IMPORTANCE Viral infection triggers the secr
171 tly higher expression of both type I and III interferons in IPEC-DQ cells than the parental rPEDV.
173 ammatory environment, characterized by serum interferon-induced protein 10 and interleukin 1alpha, is
174 sed to study the antiviral activity of IFIT (interferon-induced protein with tetratricopeptide repeat
175 d time = 6.3 days) demonstrated reduction in interferon-induced transcription, recovery of transcript
176 and higher ICAM1, VE-cadherin, occludin and interferon-induced transmembrane protein mRNAs compared
177 virus transcription, and contributes to the interferon-induced upregulation of known restriction fac
179 oamy macrophages are not proinflammatory but interferon-inducible cell and inflammatory macrophages a
181 adenylate synthetases (OASs) are a family of interferon-inducible enzymes that require double-strande
182 strin homology (PH) domains 2 (ADAP2), gamma-interferon-inducible lysosome/endosome-localized thiolre
185 y protein, endoplasmic reticulum-associated, interferon-inducible) to enhance viral infectivity.
189 e is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high e
191 Finally, we show that the clinical candidate interferon-lambda1a (IFN-lambda1a) potently inhibits SAR
192 The absence of USP18 results in unmitigated interferon-mediated inflammation and is lethal during th
193 urring picornavirus that induced a canonical interferon-mediated response and hundreds of antiviral d
194 protein that functions during NF-kappaB- and interferon-mediated signaling in response to extracellul
195 ma (IFN-gamma) and monokine induced by gamma interferon (MIG) (CXCL9) in response to mycobacterial st
196 in G (IgG) autoantibodies (auto-Abs) against interferon-omega (IFN-omega) (13 patients), against the
198 E clinical endophenotypes, with genes of the interferon pathway being highly enriched in DCEs that be
199 High viral cases have high activation of interferon pathway genes and a predominant M1-like macro
200 : Sofosbuvir (SOF)/ribavirin (RBV)/pegylated interferon (PEG-IFN), 25.2%; SOF/RBV, 62.4%; SOF/RBV/dac
202 and positive immune score as a surrogate of interferon-primed exhausted CD8 + T-cells in the tumor m
203 of characteristic biomarkers (type I and III interferons) produced by PBMCs transfected with NANPs.
205 pe I interferon-regulated genes due to lower interferon production and responsiveness, blunted STAT1
207 acytoid dendritic cells, are responsible for interferon production prior to clinical autoimmunity.
209 ts into autophagosomes, and IRF3 activation, interferon production, and antiviral activity are compro
210 G translocates to endosomes for induction of interferon production, while an alternate trafficking ro
212 uate the effect of ribavirin and recombinant interferon (RBV/rIFN) therapy on the outcomes of critica
214 cell-intrinsic Toll-like receptor and type 1 interferon receptor signaling, upregulated an IRF8-depen
215 e includes suppression of hundreds of type I interferon-regulated genes due to lower interferon produ
216 al deficiency of antiviral tumor-suppressive interferon regulatory factor 1 (IRF-1) selectively promo
218 -beta (TRIF), TRIF-related adaptor molecule, interferon regulatory factor 3 (IRF-3), receptor-interac
221 revious study found microglial expression of interferon regulatory factor 5 (IRF5) and IRF4 was relat
224 The restrictive effects of IFN-I require the interferon regulatory factor IRF5, which upregulates gen
225 h these receptors stimulates, in most cases, interferon regulatory factor-dependent type I IFN synthe
226 man herpesvirus 8 (HHV-8) encodes four viral interferon regulatory factors (vIRFs 1 to 4), all of whi
227 redominantly involves type I interferons and interferon-related genes, whereas the WT and DUBmut viru
229 ve capacity (p = 0.0005) and are more type I interferon-resistant (p = 0.007) than those transmitted
230 tified as negative regulators of the type-II interferon response (for example, Ptpn2, Socs1 and Adar1
234 onexpressing mice, but enrichment for type I interferon response gene changes was specifically observ
235 e identified inverse expression of antiviral interferon response genes (ISGs) and positive correlatio
236 ted with ICB resistance, including increased interferon response genes and glucocorticoid response ge
237 orresponds to distinct spatial expression of interferon response genes demonstrating the intra-pulmon
239 protect virus-infected cells from the type I interferon response in cells undergoing lytic virus repl
240 h nucleic acids triggers an antiviral type I interferon response in neuroglia, resulting in complemen
241 tive to uninfected cells, and disrupting the interferon response in persistently infected bat cells i
242 broad clonal T cell expansion and curtailed interferon response in severe compared with mild Neuro-C
249 these viruses and produced higher levels of interferon responses than were seen with wild-type icPED
253 e monophosphate synthase (cGAS) and enhanced interferon signaling mediated by the cGAS-stimulator of
255 ent protein binds to a protein in the type I interferon signaling pathway Tyk2 and inhibits the expre
256 fection impaired AM crawling via the type II interferon signaling pathway, and this greatly increased
259 an enrichment in the IL-12 family and type I interferon signaling pathways was observed among the set
260 pharmacologically inhibiting necroptosis or interferon signaling protects human organoids derived fr
261 unctuated by a late prenatal spike in type I interferon signaling that promotes perinatal HPC expansi
262 ted cells, EBOV downregulates STAT1 mRNA and interferon signaling, and it upregulates putative pro-vi
263 clear factor-kappaB-dependent, type I and II interferon signaling, and leukocyte activation pathways.
264 to the human disease, such as type I and II interferon signaling, cell-cell adhesion, leukocyte chem
265 in a Dectin-1 and Card9- and type I and III interferon signaling-dependent manner, respectively.
271 ro-COVID CSF leukocytes featured an enriched interferon signature; however, this was less pronounced
273 y, mediated by the expression of an array of interferon-stimulated antiviral genes, is a vital part o
274 heral blood mononuclear cells and quantified interferon-stimulated gene (ISG) expression in CD4 T cel
275 rikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway e
278 ses green fluorescent protein (GFP) under an interferon-stimulated gene promoter, we repeatedly obser
279 a high-throughput genetic screen of a human interferon-stimulated gene short-hairpin RNA library, we
280 n CHB patients, peg-IFN treatment induced an interferon-stimulated gene signature in monocytes and in
281 is a processing body (P-body) protein and an interferon-stimulated gene that can affect replication o
282 Cholesterol 25-hydroxylase (CH25H) is an interferon-stimulated gene that converts cholesterol to
283 preciated individual- and cell-type-specific interferon-stimulated gene upregulation, we describe tem
286 Here, we screen a library of nearly 400 interferon-stimulated genes (ISGs) against a biologicall
287 nd primary fibroblasts leads to induction of interferon-stimulated genes (ISGs) through JAK/STAT sign
292 in common by type I and III IFNs have strong interferon-stimulated response element (ISRE) promoter m
293 promised NS5-mediated hSTAT2 degradation and interferon suppression, and viral infection under interf
295 -AMP, which mediates the induction of type I interferons through the STING-TBK1-IRF3 signalling axis(
296 wing of TCR repertoires were associated with interferon type I and III responses, early CD4(+) and CD
298 tory cytokines, but the production of type I interferons, which are key antiviral mediators, is repor
299 l infection triggers the secretion of type I interferons, which in turn induce the expression of hund