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1 syl-uridine), alpha interferon, or pegylated alpha interferon.
2 to inhibit the antiviral response induced by alpha interferon.
3 nd E2, and HCV replication was suppressed by alpha interferon.
4 on for PKR activation in vivo in response to alpha interferon.
5 sed by production of soluble factors such as alpha interferon.
6 ufficient to render translation resistant to alpha interferon.
7 followed by maintenance therapy with DEX and alpha interferon.
8 TNF-alpha was greater than that of gamma or alpha interferon.
9 of the 2-5A system in the anti-HIV effect of alpha interferon.
10 rted to increase the therapeutic response to alpha interferon.
11 ay be preventable by treating the donor with alpha-interferon.
12 ed therapies for chronic hepatitis C are the alpha interferons.
14 Additional BLT mice were treated with human alpha interferon 2b (IFN-alpha2b) (intron A) and assesse
17 ure to proinflammatory cytokines such as TNF-alpha +/- interferon alpha/beta has marginal effects on
18 e ability of intranasal treatment with human alpha interferon (alpha-IFN) to reduce lung and nasal wa
21 and a synergistic effect was observed, with alpha interferon and interferon-inducible protein 10 und
22 orrelated with increased pulmonary levels of alpha interferon and interleukin-1beta in pigs infected
23 itis C virus (HCV) infection using pegylated alpha interferon and ribavirin leads to sustained cleara
25 virin to alpha interferon, the pegylation of alpha interferon, and the demonstration that sustained v
26 atment part, four patients were treated with alpha-interferon, and all were able to undergo the reint
27 th a Us11 mutant virus are hypersensitive to alpha interferon, arresting translation upon entry into
28 aternal antibodies and that the provision of alpha interferon as an additional signal leads to antibo
31 xamined for tumor necrosis factor alpha (TNF-alpha), interferon beta (IFN-beta), interleukin 6 (IL-6)
33 t autoantibodies directed against interferon-alpha, interferon-beta, interleukin-1alpha (IL-1alpha),
37 ere used either alone or in combination with alpha-interferon, chlorambucil, or interleukin-2 (IL-2).
38 Since human CSF-1 stimulates secretion of alpha interferon from mononuclear cells and BARF1 encode
39 (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interferon gamma (IFN-gamma), and granulocyte ma
40 n-8 (IL-8), tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), and IL-1beta in ai
42 m levels of tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), interleukin-12p40
43 ls of serum tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFNgamma), MCP-1, MCP-5, sTNRF
45 leukin (IL)-12, IL-10, tumor necrosis factor alpha, interferon gamma (IFN-gamma), and transforming gr
46 cell-derived cytokines tumor necrosis factor alpha, interferon gamma, and granulocyte/macrophage colo
47 Mean plasma levels of tumor necrosis factor alpha, interferon gamma, and interferon gamma-induced pr
49 ex vivo production of tumor necrosis factor alpha, interferon gamma, and interleukin 1beta but incre
50 al burden or levels of tumor necrosis factor alpha, interferon gamma, interleukin 6, soluble CD14, or
51 fic agonist, abrogated tumor necrosis factor alpha/interferon gamma-induced apoptosis through pathway
52 tory genes (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], and interleukin 8
53 cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], transforming growt
54 tumor necrosis factor alpha, interleukin 10, alpha interferon, gamma interferon, prostaglandins, or r
55 IL-12 p40, tumor necrosis factor alpha (TNF alpha), interferon-gamma (IFN gamma), and granulocyte-ma
56 es, such as tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and interleukin 6
57 oduction of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin 10 (IL
58 ls of serum cytokines (tumor necrosis factor-alpha, interferon-gamma and interleukin-1beta, -2, -4, -
60 kin [IL]-21, IL-1beta, tumor necrosis factor-alpha, interferon-gamma) and CCR5, HLA-DR, CD38, and Th1
61 eases in the levels of tumor necrosis factor-alpha, interferon-gamma, and active transforming growth
62 ta, IL-6, IL-10, tumor necrosis factor (TNF)-alpha, interferon-gamma, and granulocyte-macrophage colo
63 ured and production of tumor necrosis factor-alpha, interferon-gamma, and IL-10 were assessed by immu
64 ites tested for interleukin (IL)-1beta , TNF-alpha, interferon-gamma, and IL-6 was obtained from rats
65 sis highlighted the activation of Interferon-alpha, Interferon-gamma, and IL6/JAK-STAT3 signaling, al
66 s revealed decrease of tumor necrosis factor-alpha, interferon-gamma, and inducible nitric oxide synt
67 y mediators, including tumor necrosis factor alpha, interferon-gamma, and inducible nitric oxide synt
69 reas reduced levels of tumor necrosis factor-alpha, interferon-gamma, and interleukin-2 were detected
71 6, IL-9, IL-11, IL-15, tumor necrosis factor-alpha, interferon-gamma, and lipopolysaccharide fail to
73 interleukins 6 and 8, tumor necrosis factor-alpha, interferon-gamma, and matrix metalloproteinase-2
74 ng growth factor-beta, tumor necrosis factor-alpha, interferon-gamma, and MCP-1; specific cell types,
76 derived growth factor, tumor necrosis factor-alpha, interferon-gamma, and phorbol 12-myristate 13-ace
77 antly higher levels of tumor necrosis factor-alpha, interferon-gamma, and regulated on activation nor
78 in-12, interleukin-13, tumor necrosis factor-alpha, interferon-gamma, C-reactive protein, and procalc
79 of interleukin (IL)-6, tumor necrosis factor-alpha, interferon-gamma, IL-10, monocyte chemotactic pro
80 induced mice including tumor necrosis factor-alpha, interferon-gamma, interleukin (IL)-2, IL-9, IL-12
81 iver tissue, including tumor necrosis factor alpha, interferon-gamma, interleukin (IL)-6, IL-12, and
82 and chemokines such as tumor necrosis factor-alpha, interferon-gamma, interleukin 10 (IL-10), and CXC
83 uring acute rejection: tumor necrosis factor-alpha, interferon-gamma, interleukin- (IL) 1beta, IL-2,
84 evaluate inflammatory (tumor necrosis factor-alpha, interferon-gamma, interleukin-6) and alloimmune (
85 tragraft inflammation (tumor necrosis factor-alpha, interferon-gamma, interleukin-6) and alloimmune a
86 nd increased levels of tumor necrosis factor-alpha, interferon-gamma, matrix metalloproteinase (MMP)-
87 llular activation with tumor necrosis factor-alpha, interferon-gamma, or lipopolysaccharide, as shown
88 es interleukin-1alpha, tumor necrosis factor-alpha, interferon-gamma, or transforming growth factor-b
89 (i.e., interleukin-2, tumor necrosis factor-alpha, interferon-gamma, perforin, and CD107a expression
90 tion and production of tumor necrosis factor-alpha, interferon-gamma, regulated on activation normal
91 actor 2, flt-3 ligand, tumor necrosis factor alpha, interferon-gamma-inducible 10-kd protein, granulo
92 protein-1, macrophage inflammatory protein-1 alpha, interferon-gamma-inducible protein of 10 kd, KC,
94 (2) also inhibited the tumor necrosis factor-alpha-, interferon-gamma-, and interleukin-1beta-mediate
95 ng anti-(alpha)-tumor necrosis factor (TNF), alpha-interferon-gamma (IFN-gamma), or alpha-interleukin
106 identify genes required for the activity of alpha interferon (IFN-alpha) against vesicular stomatiti
107 ouble-stranded RNA, single-stranded RNA) and alpha interferon (IFN-alpha) and IFN-beta are produced.
110 le in humans, it is a potent inducer of both alpha interferon (IFN-alpha) and IFN-beta) production, a
113 inhibited the induction of multiple genes by alpha interferon (IFN-alpha) and IFN-gamma, including th
114 C(-/-) mice also displayed reduced levels of alpha interferon (IFN-alpha) and IgM in the serum, indic
115 his study, we investigated the production of alpha interferon (IFN-alpha) and inducible chemokines by
116 cause of the known stimulatory properties of alpha interferon (IFN-alpha) and interleukin-15 (IL-15),
117 ctivated by the cytokines interleukin 12 and alpha interferon (IFN-alpha) and plays a significant rol
118 only in a fraction of patients treated with alpha interferon (IFN-alpha) and ribavirin combination t
120 rom Huh-7 clones by prolonged treatment with alpha interferon (IFN-alpha) and that a higher frequency
121 lated genes (ISGs), we pretreated cells with alpha interferon (IFN-alpha) and then infected the cells
122 5-(2-bromovinyl)-2'-deoxyuridine (5BVdU) and alpha interferon (IFN-alpha) and when the antivirals are
124 ypically trigger the prodigious secretion of alpha interferon (IFN-alpha) by plasmacytoid dendritic c
126 In this study, we tested the hypothesis that alpha interferon (IFN-alpha) could improve the function
127 tical role in the production of TMEV-induced alpha interferon (IFN-alpha) during early viral infectio
128 BHK21 and Huh-7 cells and demonstrated that alpha interferon (IFN-alpha) effectively inhibited the r
129 nfection in vitro induced less IFN-gamma and alpha interferon (IFN-alpha) from CD1d-deficient splenoc
130 s (pDCs) are intrinsically unable to produce alpha interferon (IFN-alpha) in response to SIV RNA stim
132 ccumulation of HCV RNA can be inhibited with alpha interferon (IFN-alpha) in vivo and in culture cell
136 o definite cure for chronic hepatitis B, and alpha interferon (IFN-alpha) is the only available immun
137 a peak of induction that coincides with peak alpha interferon (IFN-alpha) levels in plasma, and that
139 dendritic cells (DCs) that corresponded with alpha interferon (IFN-alpha) production and a rapid decr
140 ding activity and, therefore, suppression of alpha interferon (IFN-alpha) production and IFN-mediated
141 l with regard to its potential for sustained alpha interferon (IFN-alpha) production and induction of
142 1c and CD86 as well as an increased level of alpha interferon (IFN-alpha) production compared to leve
145 ncreased levels of H1N1 replication, reduced alpha interferon (IFN-alpha) protein synthesis, and no d
147 s with Tyk2, a signaling intermediate in the alpha interferon (IFN-alpha) signaling pathway, via a pr
148 n of interferon-stimulated genes (ISGs) upon alpha interferon (IFN-alpha) stimulation in cell culture
150 is C virus (HCV) infections are resistant to alpha interferon (IFN-alpha) therapy, subgenomic in vitr
151 MLN4924 only when T cells were treated with alpha interferon (IFN-alpha) to induce high levels of BS
152 depletion rendered cells less responsive to alpha interferon (IFN-alpha) treatment by impairing IFN-
156 , we demonstrate the ability of short-course alpha interferon (IFN-alpha) treatments to effectively e
158 cordingly, BST-2 upregulation in response to alpha interferon (IFN-alpha) was shown to increase the s
160 a hybrid replicons maintained sensitivity to alpha interferon (IFN-alpha), albeit with an eightfold-h
161 L-1beta, IL-12, tumor necrosis factor alpha, alpha interferon (IFN-alpha), and IFN-beta throughout th
162 In addition, the levels of CD83, CD11b, alpha interferon (IFN-alpha), and IFN-beta, but not IFN-
163 of the production of interleukin-12 (IL-12), alpha interferon (IFN-alpha), and IFN-gamma by the Ad-in
164 in-1beta (IL-1beta), IL-6, IL-10, IL-12 p40, alpha interferon (IFN-alpha), and IFN-gamma, it actively
165 ) this anti-HIV activity is partially due to alpha interferon (IFN-alpha), but not to IFN-gamma, IFN-
166 airway fluid levels of interleukin-6 (IL-6), alpha interferon (IFN-alpha), CXCL1 (keratinocyte chemoa
168 combinant human tumor necrosis factor alpha, alpha interferon (IFN-alpha), IFN-beta, or IFN-gamma for
170 ines, including tumor necrosis factor alpha, alpha interferon (IFN-alpha), interleukin-1 beta (IL-1 b
171 d dengue virus and induced the expression of alpha interferon (IFN-alpha), key cytokines, and cell ad
172 evidenced by significantly higher levels of alpha interferon (IFN-alpha), MIP-1alpha, and MIP-1beta
173 he mRNA expression of four immune modulators-alpha interferon (IFN-alpha), oligoadenylate synthetase
174 lations that displayed partial resistance to alpha interferon (IFN-alpha), telaprevir, daclatasvir, c
175 strate hepatitis C virus (HCV) inhibition by alpha interferon (IFN-alpha), the detailed inhibition ki
176 nce HSV-1 ICP0 mutants are hypersensitive to alpha interferon (IFN-alpha), we examined the effect of
182 of MxB to the HIV-1 restriction observed in alpha interferon (IFN-alpha)-treated human cells is unkn
190 UV-killed RSV or mock conditions, contained alpha interferon (IFN-alpha; median, 43 pg/ml) and IFN-l
191 P-1beta, RANTES, tumor necrosis factor (TNF)-alpha, interferon (IFN)-alpha, IFN-gamma, granulocyte-ma
192 as increased for tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-10 a
193 H that expressed tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-10 w
194 and secretion of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-2 by
196 efine a central role for type I interferons (alpha interferon [IFN-alpha] and IFN-beta) in severe dis
197 tective roles for antiviral cytokines (e.g., alpha interferon [IFN-alpha] and IFN-gamma) against WNV
201 Based on the first decade of research on alpha interferon in viral hepatitis, one can conclude th
202 Core, NS3, and NS5A can block the action of alpha interferon in vitro; hence, these genetic patterns
206 latently infected B-cell lines they inhibit alpha interferon-induced apoptosis that is believed to b
209 ning transcription factor to be studied, the alpha-interferon-induced ISGF3, is composed of a Stat1:2
210 s sequence binding protein or IRF-7, a novel alpha interferon-inducible factor identified in this stu
211 ic variations in tumor necrosis factor (TNF)-alpha, interferon (INF)-gamma, transforming growth facto
212 chemistry, cumulative steroid, and OKT3 and alpha-interferon (INF) dose data were collected at the t
214 standard therapy of chronic hepatitis C with alpha interferon is less than ideal, numerous other appr
218 ive in double-blind trials and low dose oral alpha interferon looks promising in initial open studies
219 mice with RSV rA2 line 19F resulted in lower alpha interferon lung levels 24 h postinfection, higher
221 erved amino acid in each position of several alpha interferon nonallelic subtypes to generate a conse
222 he latent transcription factors activated by alpha interferon or gamma interferon contain the Stat1 p
223 of virological responders to either standard alpha interferon or peginterferon has demonstrated a pro
225 rimary blood mononuclear cells in vitro with alpha interferon or with Toll-like receptor (TLR) agonis
226 kine receptor inhibition; cytokine addition (alpha-interferon or interleukin-10); novel anti-metaboli
227 eloid leukemia (CML) patients, intolerant of alpha-interferon or with interferon-resistant disease.
229 , is currently treated with either pegylated alpha interferon (pegIFN-alpha) or one of the five nucle
230 ant repression of Qp activity in response to alpha interferon, possibly mediated by either the interf
231 asmacytoid dendritic cells are the principal alpha interferon-producing cells (IPC), responsible for
232 wever, pretreatment of D2-Mx1(r/r) mice with alpha interferon protected them from lethal infections.
233 enhances PDL-1 expression and does so in an alpha interferon receptor (IFNAR) signaling-dependent ma
234 which is initiated through activation of the alpha interferon receptor (IFNAR), regulates the express
239 utant BARF1 EBV showed reduced inhibition of alpha interferon secretion by human mononuclear cells wh
241 ressed from the EBV genome directly inhibits alpha interferon secretion, which may modulate the innat
243 in pediatric rheumatology, most notably the alpha interferon signature of systemic lupus erythematos
245 .003) and TRIM22 (P = 0.0006) in response to alpha interferon stimulation and increased expression of
246 ed in HEK293 cells treated with poly(I:C) or alpha interferon, suggesting a direct effect of virus in
247 to produce proinflammatory factors, such as alpha interferon, that play a critical role in inducing
248 A in the serum, the addition of ribavirin to alpha interferon, the pegylation of alpha interferon, an
253 Ribavirin (RBV), used in combination with alpha interferon to treat hepatitis C virus (HCV) infect
254 uired for wild-type levels of replication in alpha interferon-treated cells and, along with the gamma
256 rm clinical and economic outcomes of current alpha interferon treatment regimens remains limited.
257 itis C is a life-shortening disease and that alpha interferon treatment, for 6 or 12 months, despite
259 esis of antiviral, proinflammatory cytokines alpha interferon, tumor necrosis factor alpha, and inter
260 esent on the biopsy specimen, treatment with alpha-interferon was begun and the anti-TB drugs were su
262 and safety of interferon alfa-n3, a natural alpha interferon which contains multiple interferon spec