ライフサイエンスコーパス: IFN

1 IFN-alpha treatment also led to enhanced neutrophil adhe

2 IFN-gamma blocking antibody administered to Sphk2(-/-) m

3 IFN-gamma or lipopolysaccharide (LPS) polarizes macropha

4 IFN-gamma production by these lymphocytes likely plays a

5 IFN-gamma repressed genes by suppressing the function of

6 IFN-gamma treatment to GCSCs induced ZEB1 expression, at

7 IFN-gamma-inducible protein 16 (IFI16) is an immunologic

8 IFN-gamma-primed MCs guide activation of T cells by Stap

9 IFN-lambda4 acted faster than other type III IFNs in ind

10 IFN-lambda4 is a unique type III IFN because it is produ

11 IFN-related pathways have not been studied in morphea, a

12 IFN-stimulated genes were hypo-expressed in the liver of

13 IFNs are produced at high levels during viral infection

14 We discovered a significant IL-17A(+)IFN-gamma(+) (Th17/1) population and determined that the

15 IL-4, IFN-gamma, and TNF-alpha enhanced mucosal permeability i

16 ctors and output of cytokines, such as IL-4, IFN-gamma, IL-17, and IL-10.

17 inflammatory cytokines and chemokines (IL-6, IFN-gamma, TNF-alpha, CXCL1, and CCL2) and extensive spl

18 Finally, cultured fibroblasts activated IFN-gamma and IL-17A cytokine production by autologous,

19 inactivation in oligodendrocytes aggravated IFN-gamma-induced remyelinating oligodendrocyte death an

20 roduction of three key cytokines: TNF-alpha, IFN-gamma, and IL-2.

21 expression of inflammatory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6, and CCL2 mRNAs), and attenuat

22 An IFN-I signature was evident in DCs responding to the hel

23 N terminus of E3 is necessary to inhibit an IFN-primed virus-induced necroptosis.

24 renaviruses JUNV and MACV readily trigger an IFN response in a RIG-I-dependent manner.

25 d activator of transcription (STAT1), via an IFN-independent but EGFR- and integrin-dependent signali

26 is a glycosylphosphatidylinositol-anchored, IFN-inducible protein that regulates T lymphocytes proli

27 nterval [CI], 1.4,1.7], P value < .0001) and IFN-gamma ELISPOT (estimated GMFR = 2.0 [95% CI, 1.6,2.6

28 CD4 T cells were then analyzed for IL-13 and IFN-gamma expression.

29 eral blood IFN-gamma(+)IL-17(+) (TH1/17) and IFN-gamma(-)IL-17(+) (TH17) CD4(+) T cells display disti

30 ) in the bronchoalveolar fluid, and IL-2 and IFN-gamma cytokines in restimulated splenocyte cultures.

31 ein family, such as absent in melanoma-2 and IFN-gamma-inducible protein (IFI)16, bind dsDNA and form

32 IL-21 and IFN-gamma are coexpressed by Tfh cells during viral infe

33 by the endogenous cytokines IL-2, IL-4, and IFN.

34 nsferred CTLs enhances T cell activation and IFN-gamma production in vitro, leading to a significant

35 correlated well with functional activity and IFN-stimulated gene expression.

36 nd IFN-stimulated genes had higher basal and IFN-induced expression in human and mouse cerebellar ast

37 d, as exemplified by their T-bet, CXCR3, and IFN-gamma expression.

38 cytotoxic T lymphocyte-associated genes and IFN-gamma-inducible chemokines, including CXCL10, in IDH

39 ce, cGAS/cGAMP amplify both inflammasome and IFN-I to control murine cytomegalovirus.

40 The mTORC1 and IFN-gamma production defects were partially rescued by s

41 Thus, NS1 and IFN-lambda interactions govern IEC tropism and persisten

42 Pattern recognition receptors and IFN-stimulated genes had higher basal and IFN-induced ex

43 he IFN response allows viruses to antagonize IFN at multiple levels.

44 tion, effects abrogated by neutralizing anti-IFN-gamma antibodies.

45 In mice with MAS, treatment with the anti-IFN-gamma antibody significantly decreased circulating l

46 t the genomic level, less is known about bat IFN-mediated transcriptional responses.

47 differentiation, at which time cells become IFN responsive, allowing induction of a broad spectrum o

48 In the absence of T-bet, IFN-gamma aberrantly induced a type I IFN transcriptomic

49 ntagonizes the induction of interferon beta (IFN-beta) by interacting with and degrading retinoic aci

50 sensitive to inhibition by interferon beta (IFN-beta) in vitro and functions as a highly efficacious

51 us infection efficiency, decreased IFN-beta, IFN-lambda1, and interferon-stimulated chemokine gene ex

52 thmatics display overexpression of IFN-beta, IFN-lambda1/IL-29 and ISGs in their sputum cells that ma

53 studies using a monoclonal antibody to block IFN-alpha/beta receptor (IFNAR) signaling in humanized m

54 Here we show that human peripheral blood IFN-gamma(+)IL-17(+) (TH1/17) and IFN-gamma(-)IL-17(+) (

55 the response to DBP-FITC was not affected by IFN-I receptor blockade, a finding consistent with the k

56 effect of Vpu was shown to be attenuated by IFN-alpha treatment.

57 bial peptides was killed more efficiently by IFN-beta than was the wild-type S. aureus, and immunoblo

58 tivation and processing that is initiated by IFN-1, in perspective of the resulting phenotypes.

59 ing induction of a broad spectrum of ISGs by IFN signaling.

60 immunological imbalance of Tregs and CD4(+) IFN-gamma(+) cells in the lacrimal gland.

61 gnificant numbers of antigen-specific CD8(+) IFN-gamma-positive cells following injection into BALB/c

62 reased latency; and also increased CD4, CD8, IFN-gamma, and PD-1 transcripts in the TG of latently in

63 In Huh-7.5 cells, IFN treatment increased the total amount of HCV dsRNA th

64 rate, hepatic infiltration of immune cells, IFN-lambda3 expression, and serum sCD163 levels (a marke

65 re we report the characterization of chicken IFN-kappa (chIFN-kappa) near the type I IFN locus on the

66 uced by type II IFN, and the use of chimeric IFN-gamma-sensitive/resistant viruses indicates that int

67 Chronic IFN production stemmed from the accumulation of DNA in t

68 One of the crucial IFN-gamma target genes required for control of M. tuberc

69 expression of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta and RANTES and activation

70 increased production of protective cytokines IFN-gamma, TNF-alpha, and IL-12, as well as recruitment

71 Sendai virus infection efficiency, decreased IFN-beta, IFN-lambda1, and interferon-stimulated chemoki

72 y as a novel inborn error of IL-12-dependent IFN-gamma immunity associated with susceptibility to par

73 RNA Pol II recruitment to the IRF3-dependent IFN-stimulated genes (ISGs).

74 interferon (IFN)-gamma or epithelial-derived IFN-gamma in constitutively released or Porphyromonas gi

75 IFN-gamma or with conditioned media-derived IFN-gamma exhibited low levels of Cathepsin K, TRAP, RAN

76 the disease-amplifying role of Th17-derived IFN-gamma in DED pathogenesis.

77 mutations in 2 genes that regulate distinct IFN pathways.

78 Genetic ablation of either IFN-gamma signaling or T-bet expression in B cells subst

79 sus unstimulated organoid cultures, elevated IFN-gamma reduced the mRNAs encoding for RANKL, TRAP, an

80 Endogenous IFN-lambda4 protein was detectable only in Sendai virus-

81 pression patterns associated with endogenous IFN-beta.

82 Identification of excessive IFN-gamma production by blood and lymph node-derived T c

83 osed to patient plasma samples or exogeneous IFN-alpha.

84 he response to both endogenous and exogenous IFN-lambda.

85 Finally, exogenous IFN-alpha did not substantially protect cardiomyocytes a

86 te-like cells present in the liver expresses IFN-gamma and can confer protection against M. avium inf

87 psis by activating NK cells and facilitating IFN-gamma production.

88 The antiviral restriction factor IFN-induced transmembrane protein 3 (IFITM3) inhibits ce

89 ing to the source of infection, enriched for IFN signaling and antigen presentation.

90 LPS stimulation and is strongly enriched for IFN-inducible genes.

91 ptional profiling showed little evidence for IFN signature in whole blood.

92 and human lupus studies revealed a role for IFN-alpha in vascular abnormalities associated with impa

93 However, ExoN(-) virus generated from IFN-beta-pretreated cells had reduced specific infectivi

94 ent premature induction of interferon-gamma (IFN-gamma) expression in T cells and to generate pathoge

95 rowth inhibition occurs by interferon-gamma (IFN-gamma)-mediated depletion of intracellular tryptopha

96 production of the cytokine interferon-gamma (IFN-gamma).

97 by PapMV in the absence of C3 induced higher IFN-alpha production, resulting in superior immune cell

98 ct from Salmonella infection by priming host IFN-gamma responses.

99 This study addresses how IFN-gamma can suppress activation of diabetogenic CD8(+)

100 When activated in vitro, however, IFN-gamma production by naive wild type and tristetrapro

101 ocytes treated either with recombinant human IFN-gamma or with conditioned media-derived IFN-gamma ex

102 e virus (WNV) infection by regulating type I IFN (IFN-I) response.

103 Type I IFN activation is induced by pattern-recognition recepto

104 n this study, we examined the role of type I IFN and TLR trafficking and signaling in xenobiotic syst

105 ncreased rhinovirus-induced HSPA5 and type I IFN gene expression.

106 al, and confirmed the contribution of type I IFN genes to Lyme arthritis.

107 cken IFN-kappa (chIFN-kappa) near the type I IFN locus on the sex-determining Z chromosome.

108 n immunosuppression and predicts that type I IFN modulation will be pivotal to cure human chronic inf

109 ings suggest that the STING-dependent type I IFN pathway is critical for the GBP-mediated release of

110 In conclusion, the type I IFN pathway is dysfunctional at the epigenetic level in

111 response to MI by activating IRF3 and type I IFN production.

112 atment did not reduce the spontaneous type I IFN response and did not ameliorate lethal inflammation.

113 This SAM vaccine-induced type I IFN response has the potential to provide an adjuvant ef

114 However, when the type I IFN response of mice was suppressed, then the adaptive i

115 ity highlighting key paradigms of the type I IFN response.

116 important roles in the ISG15-mediated type I IFN sensitivity of HEV.

117 nduced protection is mediated through type I IFN signaling and requires monocytes in PBMCs.

118 ulatory role by negatively regulating type I IFN signaling and, thus, HEV sensitivity to type I IFN.

119 pathogen's control through sustaining type I IFN signaling in DCs.

120 For example, when type I IFN signaling was blocked by Abs in Rag1(-/-) mice, the

121 cytoplasm of host cells can initiate type I IFN signaling.

122 ory syndromes in diseases with active type I IFN signature.

123 ronic infections display a persistent type I IFN signature.

124 Increased virus replication and type I IFN specifically inhibited the response to two immunodom

125 T-bet, IFN-gamma aberrantly induced a type I IFN transcriptomic program.

126 (-) ) strain of parasites followed by type I IFN treatment increased lesion size and parasite burden,

127 ver, significant associations between type I IFN-alpha/beta protein levels with the DNA methylation s

128 d early during HIV infection and that type I IFN-associated gene signatures persist, even during ART.

129 t hypomethylation and upregulation of type I IFN-associated genes might be critical in systemic scler

130 , we confirmed these changes for five type I IFN-associated genes.

131 responses through the initiation of a type I IFN-dependent DDR.

132 ese findings identify HgIA as a novel type I IFN-independent model of systemic autoimmunity and impli

133 By obstructing the type I IFN-induced antiviral response, miR-BART16 provides a me

134 Type I IFN-mediated neutrophil activation and NET formation may

135 leads to persistently high levels of type I IFN-stimulated gene expression and to increased resistan

136 gnaling and, thus, HEV sensitivity to type I IFN.

137 tween Nb and DBP-FITC, but revealed a type-I IFN (IFN-I) signature unique to DCs from Nb-primed mice.

138 eceptors (TLR9 and TLR3) leading to a type-I IFN mediated innate immune response that is modulated by

139 alpha-helical fold characteristic of type I IFNs and bound to IFNalpha/beta receptor 1 (IFNAR1) and

140 More recently, type I IFNs were shown to be important during bacterial infecti

141 d antibacterial activities typical of type I IFNs, albeit with 100-1000-fold reduced potency compared

142 years ago, predating the evolution of type I IFNs.

143 us (WNV) infection by regulating type I IFN (IFN-I) response.

144 Nb and DBP-FITC, but revealed a type-I IFN (IFN-I) signature unique to DCs from Nb-primed mice.

145 sist a late block that is induced by type II IFN, and the use of chimeric IFN-gamma-sensitive/resista

146 IFN-lambda4 is a unique type III IFN because it is produced only in individuals who carry

147 through the constitutive release of type III IFNs (IFNlambda1 and IFNlambda2) and become resistant to

148 IFN-lambda4 acted faster than other type III IFNs in inducing antiviral genes, as well as negative re

149 pSTAT4, nuclear translocation, and impaired IFN-gamma production.

150 Importantly, IFN-gamma exposure during activation reduced the cytotox

151 The physiological role of these proteins in IFN-gamma signaling has not been clarified.

152 Infection of HIV-1 was rescued in IFN-alpha-treated myeloid cells via upregulation of CD16

153 itulating CAVD microenvironment, resulted in IFN-gamma release.

154 ultiple T-cell effector cytokines, including IFN-gamma, IL-17, and IL-21.

155 Neutralization of IL-10 increased IFN-gamma, IL-6 and TNF-alpha production and improved ba

156 creased rhinovirus replication and increased IFN-lambda levels at the gene and protein levels.

157 g by allergen-IgE immune complexes increased IFN-gamma production in B cells of allergic patients dur

158 phenotypically distinct, and that increased IFN resistance represents their most distinguishing prop

159 icient surrogates) indicated that individual IFN-gamma-induced chemokines have diverse affects and (i

160 -receptor domain-containing adapter-inducing IFN-alpha (TRIF) and nuclear factor kappaB (NF-kappaB) c

161 e maturation of Th17 cells into inflammatory IFN-gamma-coproducing effector cells.

162 SCFAs inhibited IFN-gamma and IL-17A production in peripheral blood mono

163 Interferon (IFN)-alpha treated chimpanzees and hepatitis C patients

164 pregulation in response to alpha interferon (IFN-alpha) was shown to increase the susceptibility of H

165 vealed the activation of p53 and interferon (IFN) pathways, which enforced cell cycling in quiescent

166 d Il1b mRNA levels and decreased interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and IL-1be

167 he livers of C57BL/6 mice, gamma interferon (IFN-gamma) controls intracellular Leishmania donovani in

168 pe mice were injected with gamma interferon (IFN-gamma) DNA or colony-stimulating factor 1 (CSF-1) DN

169 creased mitogen-stimulated gamma interferon (IFN-gamma) production suggested immunomodulation, which

170 this study, we report that gamma interferon (IFN-gamma) treatment, but not IFN-alpha, -beta, or -lamb

171 Effect of recombinant human interferon (IFN)-gamma or epithelial-derived IFN-gamma in constituti

172 odel and demonstrate that type I interferon (IFN) is induced early during HIV infection and that type

173 play significant roles in type I interferon (IFN) production and signalling.

174 Type I interferon (IFN) signaling engenders an antiviral state that likely

175 e with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link between reduce

176 apy (cART), low levels of type I interferon (IFN-I) signaling persist in some individuals.

177 EMT silences protective mucosal interferon (IFN)-I and III production associated with enhanced rhino

178 croglia demonstrated the role of interferon (IFN)gamma and interleukin (IL)-4 in polarizing these cel

179 The interferon (IFN) lambda 3/4 (IFNL3/4) locus, influencing innate immu

180 coinfected patients treated with interferon (IFN) and ribavirin (RBV), between 2000 and 2008.

181 , IL-4, IL-10, IL-17A, and gamma interferon [IFN-gamma]) and rendered T cells refractory to mitogen f

182 Type I interferons (IFN-1) are cytokines that affect the expression of thous

183 Type I interferons (IFN-I) are critical in antimicrobial and antitumor defen

184 Type I interferons (IFN-Is) can now be considered as the wedge that balances

185 Interferons (IFNs) are essential components of the host innate immune

186 Type I interferons (IFNs) are essential mediators of antiviral responses.

187 e induction of antiviral type I interferons (IFNs) is the major outcome of STING activation in verteb

188 es or adults, can further differentiate into IFN-gamma-producing CD4(+) T cells.

189 and to control the viral infection involving IFN-gamma secretion.

190 g2(-/-) mice, whereas Rag2(-/-) mice lacking IFN-gamma are more susceptible than either Rag2(-/-) or

191 that HIV-specific Ab responses regulate late IFN production.

192 r tryptophan levels and trended toward lower IFN-gamma levels compared to women with persisting infec

193 cells activated in such a context are mainly IFN-gamma(+), adhere to CFB, and induce their transition

194 ZBP1-mediated cell death via the RIG-I-MAVS-IFN-beta signaling axis.

195 Flow cytometry was used to measure IFN-gamma, IL-13, IL-9, IL-17, and IL-22 cytokines in CD

196 nds between subdomains SD2 and SD3 modulated IFN binding and activity in accordance with the relative

197 Moreover, IFN-lambda-mediated sterilizing immunity against murine

198 ine IL-6 in autoantibody production, but not IFN regulatory factor 7.

199 ma interferon (IFN-gamma) treatment, but not IFN-alpha, -beta, or -lambda treatment, dramatically dec

200 y T (TEM) cells that secrete IL-17A, but not IFN-gamma, was responsible for early IL-17A production.

201 treatment of PHHs with IFN-lambda4, but not IFN-lambda3, caused a strong and sustained induction of

202 ethality is prevented by genetic ablation of IFN signaling genes such as IFNAR1 and STAT1.

203 Early activation of IFN regulatory factor 3 (IRF3) and NF-kappaB was observe

204 ANK-binding kinase 1 (TBK1), an activator of IFN responses.

205 protein 1 (ZBP1)/DNA-dependent activator of IFN-regulatory factors (DAI) that contain receptor-inter

206 ployed Flow-FISH for single-tube analysis of IFN-gamma transcript and protein profile to simultaneous

207 Distributions of IFN-gamma response levels were analyzed in healthy adole

208 Ab-mediated enhancement of IFN production required Fc gamma receptor engagement, by

209 This correlated with lower frequencies of IFN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, r

210 body response, it augmented the frequency of IFN-gamma secreting total T cells, T-helper and CTLs aga

211 tion site mutants still support induction of IFN-gamma expression; however, simultaneous mutation of

212 c cell line THP-1 results in an induction of IFN-stimulated genes in these cells.

213 romoting: (i) early correlated inhibition of IFN-gamma and TNF-alpha production, along IL-10 increase

214 his was confirmed by in vitro measurement of IFN-gamma production by activated T cells.

215 was steroid-resistant, and neutralization of IFN-gamma or IL-27 significantly suppressed RSV-induced

216 transcription factors, and overexpression of IFN-beta mRNA and protein were similar in MSK1/2 and DUS

217 philic, asthmatics display overexpression of IFN-beta, IFN-lambda1/IL-29 and ISGs in their sputum cel

218 sms were implicated in the overexpression of IFN-beta: first, JNK-mediated activation of c-jun, which

219 signalling pathways and activated a panel of IFN-regulated genes, antiviral mediators and transcripti

220 pathways are both involved in the process of IFN-gamma-regulated odonto/osteogenic differentiation of

221 role for C3 in regulating the production of IFN-alpha following TLR7 activation.

222 Production of IFN-gamma and IL-27 was steroid-resistant, and neutraliz

223 s, Tbet and GATA3, and reduced production of IFN-gamma by CD8(+) T cells.

224 tic cells (cDC1) promoted ILC1 production of IFN-gamma in a STAT4-dependent manner to limit early vir

225 target mechanism that includes repression of IFN signaling.

226 pecific mechanism accounting for the role of IFN-alpha in immunosuppression and predicts that type I

227 and highlight a positive regulatory role of IFN-induced proteins in HIV-1 infection.

228 Blocking of FDC secretion of IFN-alpha restored B cell tolerance and reduced the amou

229 in the cyclic GMP-AMP synthase-stimulator of IFN genes pathway.

230 15 mg/kg every 21 days or 5 million units of IFN-alpha-2b three times per week.

231 infection (MOI) without or with IFN-beta or IFN-lambda.

232 Whether IFN-lambda3 or IFN-lambda4 protein drives this association is not known

233 shutoff and sustain the expression of other IFN inhibitors encoded by the virus.

234 activated CD4(+) Foxp3(-) (forkhead box P3) IFN-gamma(+) T cells in the heart-draining lymph nodes.

235 period and correlated with increases in PBMC IFN-alpha responses.

236 atment predictive marker for response to PEG-IFN-based therapy in chronic HCV genotype 1 infection.

237 , vaccine-induced gamma interferon-positive (IFN-gamma(+)) Gag-specific T-cell responses were dominat

238 3-IFNL4 risk haplotype that does not produce IFN-lambda4, but produces IFN-lambda3.

239 me B and maintained their ability to produce IFN-gamma.

240 t does not produce IFN-lambda4, but produces IFN-lambda3.

241 vation of a T-cell CD4+ population-producing IFN-gamma.

242 Disease-protective IFN-gamma could be derived from any lymphocyte source an

243 led to partial integrin activation, reduced IFN-I responses in WT but not CD11b-deficient mice, and

244 hat causes impaired (ds)RNA sensing, reduced IFN induction, and susceptibility to the common cold vir

245 ndent sites results in significantly reduced IFN-gamma expression.

246 ing AMPK activity also failed to up-regulate IFN-beta and TNF-alpha after treatment with DMXAA or the

247 , and Blimp-1, and that more of them secrete IFN-gamma and readily degranulate than non-ThCTL.

248 Nasal and serum IFN-inducible protein 10 (IP-10) were measured after dos

249 eated WT mice showed upregulation of several IFN-gamma-inducible genes.

250 However, the specific IFN regulated proteins responsible for the pathogenic ef

251 discrete subset of M. tuberculosis-specific IFN-gamma(+)IL-2(-)TNF-alpha(+) CD4 T cells.

252 IL-18 and are unable to optimally stimulate IFN-gamma production by NK cells.

253 DNA given by IM + EP promoted strong IFN-gamma responses and potent viral inhibition.

254 st in vitro system, we show that synergistic IFN-gamma and tumor necrosis factor (TNF) stimulation pr

255 ng the regulation of effector function by T1-IFN in human antigen-experienced CD8(+) T cells and prov

256 Type 1 interferons (T1-IFN) are known to be a constituent of the autoinflammato

257 vide a mechanism by which the presence of T1-IFN potentiates diabetogenicity within the autoimmune is

258 tions, because topical therapies that target IFN-gamma signaling in keratinocytes could be safe and e

259 dividuals who had a change in QuantiFERON-TB IFN-gamma values from less than 0.2 to greater than 0.7

260 Altogether, our results demonstrate that IFN-inducible LY6E promotes HIV-1 entry and replication

261 antimicrobial peptides, and we observed that IFN-beta can directly kill Staphylococcus aureus Further

262 In this study, we report that IFN regulatory factor 4 (Irf4) is highly expressed in mu

263 Mechanistic analyses reveal that IFN-gamma induces CD70 expression in T cells, and CD70 l

264 pe S. aureus, and immunoblotting showed that IFN-beta interacts with the bacterial cell surface.

265 Recent studies have shown that IFN-induced transmembrane (IFITM) proteins, including IF

266 thout IFN-gamma stimulation, suggesting that IFN-gamma sensitizes these leukemias to T cell killing b

267 The IFN-inducible genes included 3 transcripts involved in t

268 Although the IFN system of several bats is characterized at the genom

269 Thus, glutamine may enhance the IFN-gamma-associated immune response and reduce the rate

270 adverse events occurred in 2 patients in the IFN group, in 1 patient in the corticosteroid group, and

271 The complex regulation of the IFN response allows viruses to antagonize IFN at multipl

272 the function of a critical component of the IFN response pathway.

273 genes, as well as negative regulators of the IFN response, such as USP18 and SOCS1 Transient treatmen

274 xpansion contributes to the evolution of the IFN system and that interferomes are shaped by lineage-s

275 Parts of the IFN-beta molecular surface (especially helix 4) are cati

276 Members of the IFN-inducible PYHIN protein family, such as absent in me

277 chIFN-kappa regulated the IFN-stimulated response element signalling pathways and

278 aprolin, which we show is able to target the IFN-beta mRNA.

279 ated activation of c-jun, which binds to the IFN-beta promoter, and second, p38-mediated inactivation

280 esting a potential protective role for these IFN-gamma-producing cells.

281 as well as the expression profiles of these IFN-associated genes were confirmed.

282 n induced by T cells upon activation through IFN-gamma and TNF-alpha.

283 Thus, IFN-lambda acted as a unique immunomodulatory agent by m

284 vivo transition of pathogenic Th17 cells to IFN-gamma producers.

285 ND10 structures increase in cells exposed to IFN-beta.

286 ment, and myostatin expression was linked to IFN-beta production.

287 requires the capacity of IECs to respond to IFN-lambda.

288 Furthermore, using IFN-gamma-deficient Th17 cells, we demonstrate the disea

289 AVS, in the presence or absence of two viral IFN antagonistic proteins.

290 tastasis and s.c. tumor growth, and this was IFN-gamma dependent.

291 Whether IFN-lambda3 or IFN-lambda4 protein drives this associati

292 %), proteinuria (9%), and fatigue (7%); with IFN and octreotide, they included fatigue (27%), neutrop

293 ssion of APOBEC3A positively correlates with IFN-treatment responses in CHB patients, while NEIL3 sho

294 We found that injection of mice with IFN-gamma DNA, which enhances the development of M1 macr

295 plicities of infection (MOI) without or with IFN-beta or IFN-lambda.

296 8 and SOCS1 Transient treatment of PHHs with IFN-lambda4, but not IFN-lambda3, caused a strong and su

297 d refractoriness to further stimulation with IFN-lambda3.

298 ailure was longer with bevacizumab than with IFN (HR, 0.72; 95% CI, 0.58 to 0.89; P = .003).

299 DPSCs treated with IFN-gamma and supplemented with pyrrolidine dithiocarbam

300 including oncogenic types, by treatment with IFN-gamma, an antiviral cytokine that is released from s

301 AML and BC-CML stem cells were MHCI+ without IFN-gamma stimulation, suggesting that IFN-gamma sensiti