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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 al burden or levels of tumor necrosis factor alpha, interferon gamma, interleukin 6, soluble CD14, or
50 fic agonist, abrogated tumor necrosis factor alpha/interferon gamma-induced apoptosis through pathway
51 tory genes (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], and interleukin 8
52 cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], transforming growt
53 tumor necrosis factor alpha, interleukin 10, alpha interferon, gamma interferon, prostaglandins, or r
54 IL-12 p40, tumor necrosis factor alpha (TNF alpha), interferon-gamma (IFN gamma), and granulocyte-ma
55 es, such as tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and interleukin 6
56 oduction of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin 10 (IL
57 ls of serum cytokines (tumor necrosis factor-alpha, interferon-gamma and interleukin-1beta, -2, -4, -
59 eases in the levels of tumor necrosis factor-alpha, interferon-gamma, and active transforming growth
60 ta, IL-6, IL-10, tumor necrosis factor (TNF)-alpha, interferon-gamma, and granulocyte-macrophage colo
61 ured and production of tumor necrosis factor-alpha, interferon-gamma, and IL-10 were assessed by immu
62 ites tested for interleukin (IL)-1beta , TNF-alpha, interferon-gamma, and IL-6 was obtained from rats
63 s revealed decrease of tumor necrosis factor-alpha, interferon-gamma, and inducible nitric oxide synt
64 y mediators, including tumor necrosis factor alpha, interferon-gamma, and inducible nitric oxide synt
66 reas reduced levels of tumor necrosis factor-alpha, interferon-gamma, and interleukin-2 were detected
68 6, IL-9, IL-11, IL-15, tumor necrosis factor-alpha, interferon-gamma, and lipopolysaccharide fail to
70 interleukins 6 and 8, tumor necrosis factor-alpha, interferon-gamma, and matrix metalloproteinase-2
71 ng growth factor-beta, tumor necrosis factor-alpha, interferon-gamma, and MCP-1; specific cell types,
73 derived growth factor, tumor necrosis factor-alpha, interferon-gamma, and phorbol 12-myristate 13-ace
74 antly higher levels of tumor necrosis factor-alpha, interferon-gamma, and regulated on activation nor
75 in-12, interleukin-13, tumor necrosis factor-alpha, interferon-gamma, C-reactive protein, and procalc
76 of interleukin (IL)-6, tumor necrosis factor-alpha, interferon-gamma, IL-10, monocyte chemotactic pro
77 induced mice including tumor necrosis factor-alpha, interferon-gamma, interleukin (IL)-2, IL-9, IL-12
78 iver tissue, including tumor necrosis factor alpha, interferon-gamma, interleukin (IL)-6, IL-12, and
79 and chemokines such as tumor necrosis factor-alpha, interferon-gamma, interleukin 10 (IL-10), and CXC
80 uring acute rejection: tumor necrosis factor-alpha, interferon-gamma, interleukin- (IL) 1beta, IL-2,
81 evaluate inflammatory (tumor necrosis factor-alpha, interferon-gamma, interleukin-6) and alloimmune (
82 tragraft inflammation (tumor necrosis factor-alpha, interferon-gamma, interleukin-6) and alloimmune a
83 nd increased levels of tumor necrosis factor-alpha, interferon-gamma, matrix metalloproteinase (MMP)-
84 llular activation with tumor necrosis factor-alpha, interferon-gamma, or lipopolysaccharide, as shown
85 es interleukin-1alpha, tumor necrosis factor-alpha, interferon-gamma, or transforming growth factor-b
86 (i.e., interleukin-2, tumor necrosis factor-alpha, interferon-gamma, perforin, and CD107a expression
87 tion and production of tumor necrosis factor-alpha, interferon-gamma, regulated on activation normal
88 actor 2, flt-3 ligand, tumor necrosis factor alpha, interferon-gamma-inducible 10-kd protein, granulo
89 protein-1, macrophage inflammatory protein-1 alpha, interferon-gamma-inducible protein of 10 kd, KC,
90 (2) also inhibited the tumor necrosis factor-alpha-, interferon-gamma-, and interleukin-1beta-mediate
91 ng anti-(alpha)-tumor necrosis factor (TNF), alpha-interferon-gamma (IFN-gamma), or alpha-interleukin
101 ouble-stranded RNA, single-stranded RNA) and alpha interferon (IFN-alpha) and IFN-beta are produced.
104 le in humans, it is a potent inducer of both alpha interferon (IFN-alpha) and IFN-beta) production, a
107 inhibited the induction of multiple genes by alpha interferon (IFN-alpha) and IFN-gamma, including th
108 C(-/-) mice also displayed reduced levels of alpha interferon (IFN-alpha) and IgM in the serum, indic
109 his study, we investigated the production of alpha interferon (IFN-alpha) and inducible chemokines by
110 cause of the known stimulatory properties of alpha interferon (IFN-alpha) and interleukin-15 (IL-15),
111 ctivated by the cytokines interleukin 12 and alpha interferon (IFN-alpha) and plays a significant rol
112 only in a fraction of patients treated with alpha interferon (IFN-alpha) and ribavirin combination t
114 rom Huh-7 clones by prolonged treatment with alpha interferon (IFN-alpha) and that a higher frequency
115 lated genes (ISGs), we pretreated cells with alpha interferon (IFN-alpha) and then infected the cells
117 ypically trigger the prodigious secretion of alpha interferon (IFN-alpha) by plasmacytoid dendritic c
119 tical role in the production of TMEV-induced alpha interferon (IFN-alpha) during early viral infectio
120 BHK21 and Huh-7 cells and demonstrated that alpha interferon (IFN-alpha) effectively inhibited the r
121 nfection in vitro induced less IFN-gamma and alpha interferon (IFN-alpha) from CD1d-deficient splenoc
122 s (pDCs) are intrinsically unable to produce alpha interferon (IFN-alpha) in response to SIV RNA stim
124 ccumulation of HCV RNA can be inhibited with alpha interferon (IFN-alpha) in vivo and in culture cell
128 a peak of induction that coincides with peak alpha interferon (IFN-alpha) levels in plasma, and that
130 dendritic cells (DCs) that corresponded with alpha interferon (IFN-alpha) production and a rapid decr
131 ding activity and, therefore, suppression of alpha interferon (IFN-alpha) production and IFN-mediated
132 l with regard to its potential for sustained alpha interferon (IFN-alpha) production and induction of
133 1c and CD86 as well as an increased level of alpha interferon (IFN-alpha) production compared to leve
136 ncreased levels of H1N1 replication, reduced alpha interferon (IFN-alpha) protein synthesis, and no d
137 s with Tyk2, a signaling intermediate in the alpha interferon (IFN-alpha) signaling pathway, via a pr
139 is C virus (HCV) infections are resistant to alpha interferon (IFN-alpha) therapy, subgenomic in vitr
140 MLN4924 only when T cells were treated with alpha interferon (IFN-alpha) to induce high levels of BS
141 depletion rendered cells less responsive to alpha interferon (IFN-alpha) treatment by impairing IFN-
146 cordingly, BST-2 upregulation in response to alpha interferon (IFN-alpha) was shown to increase the s
148 a hybrid replicons maintained sensitivity to alpha interferon (IFN-alpha), albeit with an eightfold-h
149 L-1beta, IL-12, tumor necrosis factor alpha, alpha interferon (IFN-alpha), and IFN-beta throughout th
150 In addition, the levels of CD83, CD11b, alpha interferon (IFN-alpha), and IFN-beta, but not IFN-
151 of the production of interleukin-12 (IL-12), alpha interferon (IFN-alpha), and IFN-gamma by the Ad-in
152 in-1beta (IL-1beta), IL-6, IL-10, IL-12 p40, alpha interferon (IFN-alpha), and IFN-gamma, it actively
153 ) this anti-HIV activity is partially due to alpha interferon (IFN-alpha), but not to IFN-gamma, IFN-
154 airway fluid levels of interleukin-6 (IL-6), alpha interferon (IFN-alpha), CXCL1 (keratinocyte chemoa
156 combinant human tumor necrosis factor alpha, alpha interferon (IFN-alpha), IFN-beta, or IFN-gamma for
158 ines, including tumor necrosis factor alpha, alpha interferon (IFN-alpha), interleukin-1 beta (IL-1 b
159 d dengue virus and induced the expression of alpha interferon (IFN-alpha), key cytokines, and cell ad
160 evidenced by significantly higher levels of alpha interferon (IFN-alpha), MIP-1alpha, and MIP-1beta
161 he mRNA expression of four immune modulators-alpha interferon (IFN-alpha), oligoadenylate synthetase
162 lations that displayed partial resistance to alpha interferon (IFN-alpha), telaprevir, daclatasvir, c
163 strate hepatitis C virus (HCV) inhibition by alpha interferon (IFN-alpha), the detailed inhibition ki
164 nce HSV-1 ICP0 mutants are hypersensitive to alpha interferon (IFN-alpha), we examined the effect of
170 of MxB to the HIV-1 restriction observed in alpha interferon (IFN-alpha)-treated human cells is unkn
178 UV-killed RSV or mock conditions, contained alpha interferon (IFN-alpha; median, 43 pg/ml) and IFN-l
179 P-1beta, RANTES, tumor necrosis factor (TNF)-alpha, interferon (IFN)-alpha, IFN-gamma, granulocyte-ma
180 as increased for tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-10 a
181 H that expressed tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-10 w
182 and secretion of tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-2 by
184 efine a central role for type I interferons (alpha interferon [IFN-alpha] and IFN-beta) in severe dis
185 tective roles for antiviral cytokines (e.g., alpha interferon [IFN-alpha] and IFN-gamma) against WNV
189 Based on the first decade of research on alpha interferon in viral hepatitis, one can conclude th
190 Core, NS3, and NS5A can block the action of alpha interferon in vitro; hence, these genetic patterns
194 latently infected B-cell lines they inhibit alpha interferon-induced apoptosis that is believed to b
197 ning transcription factor to be studied, the alpha-interferon-induced ISGF3, is composed of a Stat1:2
198 s sequence binding protein or IRF-7, a novel alpha interferon-inducible factor identified in this stu
199 ic variations in tumor necrosis factor (TNF)-alpha, interferon (INF)-gamma, transforming growth facto
200 chemistry, cumulative steroid, and OKT3 and alpha-interferon (INF) dose data were collected at the t
202 standard therapy of chronic hepatitis C with alpha interferon is less than ideal, numerous other appr
206 ive in double-blind trials and low dose oral alpha interferon looks promising in initial open studies
207 mice with RSV rA2 line 19F resulted in lower alpha interferon lung levels 24 h postinfection, higher
209 erved amino acid in each position of several alpha interferon nonallelic subtypes to generate a conse
210 he latent transcription factors activated by alpha interferon or gamma interferon contain the Stat1 p
211 of virological responders to either standard alpha interferon or peginterferon has demonstrated a pro
213 rimary blood mononuclear cells in vitro with alpha interferon or with Toll-like receptor (TLR) agonis
214 kine receptor inhibition; cytokine addition (alpha-interferon or interleukin-10); novel anti-metaboli
215 eloid leukemia (CML) patients, intolerant of alpha-interferon or with interferon-resistant disease.
217 , is currently treated with either pegylated alpha interferon (pegIFN-alpha) or one of the five nucle
218 ant repression of Qp activity in response to alpha interferon, possibly mediated by either the interf
219 asmacytoid dendritic cells are the principal alpha interferon-producing cells (IPC), responsible for
220 wever, pretreatment of D2-Mx1(r/r) mice with alpha interferon protected them from lethal infections.
221 enhances PDL-1 expression and does so in an alpha interferon receptor (IFNAR) signaling-dependent ma
222 which is initiated through activation of the alpha interferon receptor (IFNAR), regulates the express
227 utant BARF1 EBV showed reduced inhibition of alpha interferon secretion by human mononuclear cells wh
229 ressed from the EBV genome directly inhibits alpha interferon secretion, which may modulate the innat
231 in pediatric rheumatology, most notably the alpha interferon signature of systemic lupus erythematos
233 .003) and TRIM22 (P = 0.0006) in response to alpha interferon stimulation and increased expression of
234 ed in HEK293 cells treated with poly(I:C) or alpha interferon, suggesting a direct effect of virus in
235 to produce proinflammatory factors, such as alpha interferon, that play a critical role in inducing
236 A in the serum, the addition of ribavirin to alpha interferon, the pegylation of alpha interferon, an
241 Ribavirin (RBV), used in combination with alpha interferon to treat hepatitis C virus (HCV) infect
242 uired for wild-type levels of replication in alpha interferon-treated cells and, along with the gamma
244 rm clinical and economic outcomes of current alpha interferon treatment regimens remains limited.
245 itis C is a life-shortening disease and that alpha interferon treatment, for 6 or 12 months, despite
247 esis of antiviral, proinflammatory cytokines alpha interferon, tumor necrosis factor alpha, and inter
248 esent on the biopsy specimen, treatment with alpha-interferon was begun and the anti-TB drugs were su
250 and safety of interferon alfa-n3, a natural alpha interferon which contains multiple interferon spec
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