ライフサイエンスコーパス: tumour necrosis

1 s has been reported to induce the release of tumour necrosis alpha (TNF-alpha), which may display aut

2 1 IIIB) was compared to the neurotoxin human tumour necrosis alpha (TNFalpha) on human brain cells in

3 s revealed a significant correlation between tumour necrosis and elastic modulus (r = -0.73, p = 0.02

4 ed in extensive angiogenesis, proliferation, tumour necrosis and recruitment of pro-inflammatory cell

5 Moreover, in RGC cultures, exogenous tumour necrosis- converting enzyme (TACE) initiates RIP

6 The tumour necrosis factor (TNF) -308G-->A polymorphism was

7 Anti-tumour necrosis factor (TNF) agents have revolutionized

8 ently treated with differentiation medium or tumour necrosis factor (TNF) alpha (50 ng/mL).

9 Among these, the cytokines tumour necrosis factor (TNF) alpha, interleukin (IL)-1be

10 JDM patients with anti-p140 antibodies and tumour necrosis factor (TNF) alpha-308AA allele are at a

11 ement of inflammatory cytokines, for example tumour necrosis factor (TNF) and interleukins (IL), in n

12 ad been previously treated with at least one tumour necrosis factor (TNF) antagonist (which had faile

13 fying anti-rheumatic drugs (DMARDs), such as tumour necrosis factor (TNF) antagonists, is associated

14 fe to death.The molecular switch between how tumour necrosis factor (TNF) controls inflammation versu

15 with rheumatoid arthritis treated with anti-tumour necrosis factor (TNF) drugs do not respond becaus

16 entially induce rheumatic diseases were anti-tumour necrosis factor (TNF) drugs, oncology drugs, prop

17 Tumour necrosis factor (TNF) inhibition and B-cell deple

18 rials have confirmed the role of alternative tumour necrosis factor (TNF) inhibitors (TNFi), rituxima

19 ll death (apoptosis) induced by the cytokine tumour necrosis factor (TNF) is inhibited by several ade

20 LyS, BAFF, TALL-1, THANK) is a member of the tumour necrosis factor (TNF) ligand family that is a pot

21 The tumour necrosis factor (TNF) ligand TALL-1 and its cogna

22 glucocorticoids and an antimetabolite, anti-tumour necrosis factor (TNF) monoclonal antibodies have

23 esponding to the lymphotoxin alpha (LTA) and tumour necrosis factor (TNF) promoter regions, a CpG isl

24 dl gene, which encodes a novel member of the tumour necrosis factor (Tnf) receptor (Tnfr) family.

25 itin ligases that are critical regulators of tumour necrosis factor (TNF) receptor (TNFR)-mediated si

26 Members of the tumour necrosis factor (TNF) receptor family exert pleio

27 CD40, a tumour necrosis factor (TNF) receptor family member, is

28 ess (Dl) encodes Edar, a novel member of the tumour necrosis factor (TNF) receptor family, containing

29 Members of the tumour necrosis factor (TNF) receptor superfamily have i

30 ent and selection, such as the importance of tumour necrosis factor (TNF) receptor superfamily member

31 Novel markers from the tumour necrosis factor (TNF) receptor superfamily were a

32 Here we show that tumour necrosis factor (TNF) receptor-associated factor

33 Further analyses demonstrated that tumour necrosis factor (TNF) receptor-associated factor

34 linear ubiquitin chains and is important for tumour necrosis factor (TNF) signaling activation.

35 as well as NF-kappaB sensitivity to CD40 or tumour necrosis factor (TNF) stimulation.

36 ediated by proinflammatory cytokines such as tumour necrosis factor (TNF), exacerbating tissue damage

37 icantly attenuated the release of cytokines (tumour necrosis factor (TNF), interleukin (IL)-1beta, IL

38 nes such as transforming growth factor-beta, tumour necrosis factor (TNF), interleukin-1 (IL-1) and w

39 , RIPK3, TRIF and ZBP1/DAI and inhibition of tumour necrosis factor (TNF), lipopolysaccharide or poly

40 Despite expanding use of drugs blocking tumour necrosis factor (TNF), their precise mechanisms o

41 n of RNF11 with siRNA resulted in persistent tumour necrosis factor (TNF)- and lipopolysaccharide (LP

42 In particular, death ligands such as tumour necrosis factor (TNF)-alpha activate necrosis by

43 g factor (G-CSF), interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha concentrations were h

44 ion was very variable, the 24 h secretion of tumour necrosis factor (TNF)-alpha correlated with the 8

45 Tumour necrosis factor (TNF)-alpha is a pro-inflammatory

46 nistically, Met is induced by tumour-derived tumour necrosis factor (TNF)-alpha or other inflammatory

47 e purified protein itself sharply suppressed tumour necrosis factor (TNF)-alpha release by phagocytes

48 nes (IL-2, IL-12, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha) was suppressed.

49 neys to stimulate blood monocytes to release tumour necrosis factor (TNF)-alpha, and examined the com

50 lity to induce the proinflammatory cytokines tumour necrosis factor (TNF)-alpha, interleukin (IL)-1be

51 also abrogates the binding of NEMO to RIP in tumour necrosis factor (TNF)-alpha-stimulated cells, the

52 Tumour necrosis factor (TNF)-induced hypotension and mor

53 ABIN-1 deficient cells are hypersensitive to tumour necrosis factor (TNF)-induced programmed cell dea

54 Particularly, the inflammatory cytokine tumour necrosis factor (TNF)-like weak inducer of apopto

55 Tumour necrosis factor (TNF)-receptor-associated factors

56 In the case of apoptosis mediated by TRAIL (tumour necrosis factor (TNF)-related apoptosis-inducing

57 fined mediator of contractile dysfunction is tumour necrosis factor (TNF).

58 1beta, IL-1 receptor antagonist (IL-1ra) and tumour necrosis factor (TNF).

59 clude variation of MHC and cytokines such as tumour necrosis factor (TNF).

60 FGF), with some induction also observed with tumour necrosis factor (TNF).

61 s involved in the activation of NF-kappaB by tumour necrosis factor (TNF).

62 n cancer cells treated with a short pulse of Tumour Necrosis Factor (TNF).

63 ines such as interferon-alpha (IFNalpha) and tumour necrosis factor (TNF).

64 in-1 (adjusted OR 9.0 [95% CI 1.0-80.0]) and tumour necrosis factor (TNF)alpha (7.8 [1.1-55.2]).

65 nhanced NFkappaB transcription and inhibited tumour necrosis factor (TNF)alpha-induced apoptosis.

66 Inflammatory cytokines (tumour necrosis factor [TNF]-alpha, transforming growth

67 holine to promote barrier function, new anti-tumour necrosis factor agents, B-cell (anti-CD20) deplet

68 50, p<0.0001), C5a (48%, n=41, p=0.0005), or tumour necrosis factor alpha (52%, n=27, p<0.0001).

69 and CD8; (ii) profiled cytokine production [tumour necrosis factor alpha (TNF alpha), transforming g

70 everal other extracellular signals including tumour necrosis factor alpha (TNF-alpha) and amyloid bet

71 ls of Abeta42 or the inflammatory cytokines, tumour necrosis factor alpha (TNF-alpha) and interleukin

72 e as 20 microg kg(-1) siRNA directed against tumour necrosis factor alpha (Tnf-alpha) depleted its me

73 Since tumour necrosis factor alpha (TNF-alpha) is thought to h

74 of the gene for the proinflammatory cytokine tumour necrosis factor alpha (TNF-alpha) leads to increa

75 and NC cohorts underwent serum analysis for tumour necrosis factor alpha (TNF-alpha) levels.

76 We found that FOs (0.1-100 mug/ml) induced tumour necrosis factor alpha (TNF-alpha), IL-1beta, IL-6

77 ion of a broad range of cytokines, including tumour necrosis factor alpha (TNF-alpha), interleukin (I

78 transgenic line whose macrophages expressing tumour necrosis factor alpha (tnfa), a key feature of cl

79 escalation during the 12 study weeks to anti-tumour necrosis factor alpha (TNFalpha) agents, immunomo

80 human aortic endothelial cells treated with tumour necrosis factor alpha (TNFalpha) and MAC-conditio

81 nic wound biomarkers interleukin 6 (IL6) and tumour necrosis factor alpha (TNFalpha) are used.

82 inical studies have identified and validated tumour necrosis factor alpha (TNFalpha) as a key disease

83 Further, we identified tumour necrosis factor alpha (TNFalpha) as an ototoxic m

84 f NF-kappaB present in nuclear extracts from tumour necrosis factor alpha (TNFalpha) exposed cells is

85 Tumour necrosis factor alpha (TNFalpha) is a potent cyto

86 rowth factor binding protein-3 (IGFBP-3) and tumour necrosis factor alpha (TNFalpha) on growth, diffe

87 However, both EGF and nafenopin require tumour necrosis factor alpha (TNFalpha) signalling to in

88 ity-score matching tested the effect of anti-tumour necrosis factor alpha (TNFalpha) therapy exposure

89 Plasma tumour necrosis factor alpha (TNFalpha) was increased in

90 Tumour necrosis factor alpha (TNFalpha), named for its a

91 ects these cells from apoptotic challenge by tumour necrosis factor alpha (TNFalpha).

92 markedly increased following treatment with tumour necrosis factor alpha (TNFalpha).

93 ression is induced in non-lymphoid organs by tumour necrosis factor alpha (TNFalpha).

94 turn is required to drive the expression of tumour necrosis factor alpha (TNFalpha).

95 who were not given medication showed higher tumour necrosis factor alpha (TNFalpha; SMD 0.69, 95% CI

96 d chemokines, as well as therapies to oppose tumour necrosis factor alpha and increase interleukin 10

97 We investigated the ability of inhibitors of tumour necrosis factor alpha and interleukin 1 to reduce

98 have definitively proven a critical role for tumour necrosis factor alpha and interleukin 6 in diseas

99 n tyrosine phosphatase, nonreceptor type 22, tumour necrosis factor alpha and interleukin-1 genes.

100 ds such as ranibizumab and bevacizumab, anti-tumour necrosis factor alpha antibodies such as inflixim

101 etanercept (trade name, Enbrel), which is a tumour necrosis factor alpha blocker currently used to t

102 ression correlated with synovitis as well as tumour necrosis factor alpha expression, and was induced

103 nsequence of production of the adipocytokine tumour necrosis factor alpha from the cuff of fat seen s

104 We also demonstrate that tumour necrosis factor alpha greatly potentiates agonist

105 OX2 induction by the colon tumour promoters, tumour necrosis factor alpha or fecapentaene-12.

106 ntact and competent in terms of IL-12p70 and tumour necrosis factor alpha production, induction of T-

107 T lymphocytes that proliferated and produced tumour necrosis factor alpha upon ex-vivo exposure to NA

108 luding the targeting of immunoglobulin E and tumour necrosis factor alpha with biological agents, emp

109 s on the prototypic proinflammatory cytokine tumour necrosis factor alpha, because recent studies of

110 Tumour necrosis factor alpha, dendritic cells, and T-cel

111 f septic arthritis and examine host factors (tumour necrosis factor alpha, interleukins 1 and 10) and

112 Tumour necrosis factor alpha, vascular cell adhesion mol

113 are required for ARF-induced sensitivity to tumour necrosis factor alpha-induced cell death.

114 We focus on the synergy between tumour necrosis factor and an adenoviral vector as a the

115 ts are associated with induced expression of tumour necrosis factor and IL-1beta consistent with a br

116 Injection of tumour necrosis factor and interferon gamma into the sub

117 sclerosis were used to study the presence of tumour necrosis factor and interferon gamma protein and

118 expression of the pro-inflammatory cytokines tumour necrosis factor and interferon gamma was found in

119 receptors for the proinflammatory cytokines tumour necrosis factor and interleukin-1 are crucial for

120 gulation of pro-inflammatory cytokines (e.g. tumour necrosis factor and interleukin-1beta) and pro-in

121 proinflammatory cytokines interferon gamma, tumour necrosis factor and interleukin-6 are released by

122 ction of autophagy is mediated by Drosophila tumour necrosis factor and interleukin-6-like signalling

123 The first of these to enter the clinic, tumour necrosis factor antagonists, have shown encouragi

124 d with traditional DMARD-experienced or anti-tumour necrosis factor biological drug-experienced patie

125 unequivocally demonstrated by the success of tumour necrosis factor blockade in clinical practice.

126 Treatment with XPro1595, a selective soluble tumour necrosis factor blocker, improves the clinical ou

127 Partial and non-responses to tumour necrosis factor blocking agents, however, togethe

128 Anti-tumour necrosis factor drugs were most commonly studied

129 Tumour necrosis factor exists in two biologically active

130 a secreted pro-inflammatory cytokine of the tumour necrosis factor family, to regulate TWEAK-induced

131 rol in rheumatoid arthritis, and blockade of tumour necrosis factor has the potential to protect join

132 nstrate that selective inhibition of soluble tumour necrosis factor improves recovery following exper

133 okines interleukin-6, chemokine ligand 2 and tumour necrosis factor in joint tissue.

134 rapy (typically methotrexate combined with a tumour necrosis factor inhibitor).

135 Tumour necrosis factor inhibitors (TNFi) and other biolo

136 Patients who have had inadequate response to tumour necrosis factor inhibitors have fewer treatment o

137 Tumour necrosis factor inhibitors were the first biologi

138 nd who had previously inadequate response to tumour necrosis factor inhibitors, with a safety profile

139 had loss of efficacy, or were intolerant to tumour necrosis factor inhibitors.

140 rthritis and previous inadequate response to tumour necrosis factor inhibitors.

141 nd that signalling mediated by transmembrane tumour necrosis factor is essential for axon and myelin

142 Tumour necrosis factor is linked to the pathophysiology

143 we show that selective inhibition of soluble tumour necrosis factor is therapeutic in experimental au

144 nd critical functions such as involvement in tumour necrosis factor pathways, map to a distal portion

145 ws similarity to two separate domains of the tumour necrosis factor receptor (TNFR) family.

146 Proteins that directly regulate tumour necrosis factor receptor (TNFR) signalling have c

147 CD40, a member of the tumour necrosis factor receptor (TNFR) superfamily, has

148 CD40, a member of tumour necrosis factor receptor (TNFR) superfamily, has

149 Ablation of tumour necrosis factor receptor (TNFR)-1/-2, Myeloid Dif

150 is is the first structure of a virus-encoded tumour necrosis factor receptor (TNFR).

151 of necroptosis in PDA, including ligation of tumour necrosis factor receptor 1 (TNFR1), CD95, TNF-rel

152 ism (SNP) in the TNFRSF1A gene, that encodes tumour necrosis factor receptor 1 (TNFR1), which was dis

153 erimental autoimmune encephalomyelitis shows tumour necrosis factor receptor 1 expression in neurons,

154 (myel-KO) mice is not rescued by deletion of tumour necrosis factor receptor 1.

155 rons, oligodendrocytes and astrocytes, while tumour necrosis factor receptor 2 is localized in oligod

156 CD40 is a tumour necrosis factor receptor family member that is ov

157 mmune deficiency (IMD) pathway resembles the tumour necrosis factor receptor network in mammals and s

158 uggesting that pharmacological modulation of tumour necrosis factor receptor signalling may represent

159 date genes located within this region is the tumour necrosis factor receptor superfamily member 1B (T

160 CD30, a member of the tumour necrosis factor receptor superfamily, is overexpr

161 o-acid sequence similarity to members of the tumour necrosis factor receptor superfamily.

162 certain characteristics with members of the tumour necrosis factor receptor superfamily.

163 s translocation of a TLR signalling adaptor, tumour necrosis factor receptor-associated factor 6 (TRA

164 Anti-IL-1 therapy is effective in tumour necrosis factor receptor-associated periodic synd

165 sophila, immune deficiency (IMD) signalling (tumour necrosis factor receptor/interleukin-1 receptor,

166 Immunohistochemical characterization of tumour necrosis factor receptors in the spinal cord foll

167 A group of genes in the tumour necrosis factor signalling pathway are mutated in

168 Eiger, a tumour necrosis factor superfamily ligand, appears to be

169 ed to upregulation of eiger, a member of the tumour necrosis factor superfamily of ligands, and the c

170 to show that timely escalation with an anti-tumour necrosis factor therapy on the basis of clinical

171 as non-selective inhibition of both forms of tumour necrosis factor with etanercept does not result i

172 TRAIL (TNF (tumour necrosis factor)-related apoptosis-inducing ligan

173 is and psoriasis are disease states in which tumour necrosis factor, a proinflammatory cytokine, is p

174 g interferon alpha/beta (IFN-alpha/beta) and tumour necrosis factor, but the mechanism has been uncle

175 encapsulated inflammatory mediators such as tumour necrosis factor, replicate attributes of MCs in v

176 ematic DNA footprinting of the TNF (encoding tumour necrosis factor, TNF) promoter region, we have id

177 stem (% CD16+CD14+ monocytes, interleukin-6, tumour necrosis factor-a and colony-stimulating factor 3

178 a (26.3%, 39.5% and 21.6%, respectively) and tumour necrosis factor-alpha (50.2%, 47.5% and 33.3%, re

179 LPS infusion induced increases in muscle tumour necrosis factor-alpha (8.9-fold, P < 0.001) and i

180 Tumour necrosis factor-alpha (TNF) expression is increas

181 The effects of tumour necrosis factor-alpha (TNF) on guinea-pig bronchi

182 Addition of NO gas or tumour necrosis factor-alpha (TNF-alpha) also resulted i

183 entration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin

184 the mtfD mutant show elevated production of tumour necrosis factor-alpha (TNF-alpha) and RANTES comp

185 ation, and resistance to necrosis induced by tumour necrosis factor-alpha (TNF-alpha) and related fam

186 actericidal function and lead to toxicity of tumour necrosis factor-alpha (TNF-alpha) and to pulmonar

187 further that SIRT6 promotes the secretion of tumour necrosis factor-alpha (TNF-alpha) by removing the

188 mitogen-activated protein kinase (MAPK) and tumour necrosis factor-alpha (TNF-alpha) converting enzy

189 Tumour necrosis factor-alpha (TNF-alpha) deficient mice

190 h siRNA against the proinflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) diminish TNF-al

191 Tumour necrosis factor-alpha (TNF-alpha) has been report

192 Tumour necrosis factor-alpha (TNF-alpha) is a proinflamm

193 ective of this investigation was to quantify Tumour Necrosis Factor-alpha (TNF-alpha) on-chip within

194 with features of macrophages), which promote tumour necrosis factor-alpha (TNF-alpha) production, col

195 The proinflammatory cytokine tumour necrosis factor-alpha (TNF-alpha) regulates immun

196 sed to cellular stresses, or stimulated with tumour necrosis factor-alpha (TNF-alpha), interleukin-1

197 Tumour necrosis factor-alpha (TNF-alpha), which is eleva

198 The percentage of tumour necrosis factor-alpha (TNF-alpha)-positive T cell

199 gulate pro-inflammatory target genes such as tumour necrosis factor-alpha (TNF-alpha).

200 and 10 studies including 881 individuals for tumour necrosis factor-alpha (TNF-alpha).

201 e 2 (COX-2)] and/or stimulating translation [tumour necrosis factor-alpha (TNF-alpha)] of their mRNAs

202 circulation and induced increases in muscle tumour necrosis factor-alpha (TNF-alpha; 10-fold, P < 0.

203 hed that strong, continuous stimulation with tumour necrosis factor-alpha (TNFalpha) can induce susta

204 e-only [MCT], tryptase + chymase [MCTC]) and tumour necrosis factor-alpha (TNFalpha) expression, and

205 We tested the hypothesis that spinal tumour necrosis factor-alpha (TNFalpha) is necessary for

206 Here we identify that tumour necrosis factor-alpha (TNFalpha) selectively redu

207 on of the major inflammatory cytokines (i.e. tumour necrosis factor-alpha and interleukin-1) and othe

208 -2, prostaglandin E2, prostanoid receptor-1, tumour necrosis factor-alpha and interleukin-1beta were

209 thelium with the pro-inflammatory cytokines, tumour necrosis factor-alpha and interleukin-1beta, resu

210 ffects of pro-inflammatory cytokines such as tumour necrosis factor-alpha and interleukin-1beta.

211 changes were preceded by marked increases in tumour necrosis factor-alpha and interleukin-6 mRNA expr

212 d reactive nitrogen intermediates as well as tumour necrosis factor-alpha and monocyte chemoattractan

213 Conversely, tumour necrosis factor-alpha antagonism did not affect c

214 Hence, prostanoid receptor-1 and tumour necrosis factor-alpha are downstream to cyclooxyg

215 tokines interleukin-1beta, interleukin-6, or tumour necrosis factor-alpha are significantly upregulat

216 While tumour necrosis factor-alpha contributes to inflammation

217 approach to delineate the role of ADAM10 and tumour necrosis factor-alpha converting enzyme (TACE; AD

218 The anti-tumour necrosis factor-alpha infliximab and adalimumab h

219 Cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha inhibition reduced inflamma

220 Tumour necrosis factor-alpha is a critical factor for TP

221 or prostanoid receptor-1 inhibition reduced tumour necrosis factor-alpha level, but not interleukin-

222 nd IL-4 levels and the decrease in IL-12 and tumour necrosis factor-alpha levels, normally seen with

223 y 'hybrid' phosphorothioate-LNA ODNs induces tumour necrosis factor-alpha production in the macrophag

224 the nuclear factor NF-kappaB and stimulates tumour necrosis factor-alpha production.

225 Tumour necrosis factor-alpha receptor knockout (KO) mice

226 e Traf2 gene that is known to play a role in tumour necrosis factor-alpha signalling but has not been

227 Anti-tumour necrosis factor-alpha therapies have set a new st

228 N13 microglia cells, by inducing TNF-alpha (tumour necrosis factor-alpha) expression, which plays a

229 d augmented toxin-induced increases in pouch tumour necrosis factor-alpha, IL-1beta, and especially I

230 dritic-cell-derived interleukin-12/23p40 and tumour necrosis factor-alpha, increased levels of CD4+ T

231 Thus, agents that suppress the expression of tumour necrosis factor-alpha, interleukin-1beta, cycloox

232 pokines (including leptin, free fatty acids, tumour necrosis factor-alpha, interleukin-6, C-reactive

233 a fundamental role and cytokines, especially tumour necrosis factor-alpha, participate in this proces

234 lecules, most prominently glutamate, ATP and tumour necrosis factor-alpha, whereas neurons themselves

235 ipid A stimulated human monocytes to secrete tumour necrosis factor-alpha, whereas the lipid A synthe

236 d CNA significantly reduced serum leptin and tumour necrosis factor-alpha, while modulating the mRNA

237 Here we show that the potent tumour necrosis factor-alpha-, interleukin-12- and nitri

238 wnstream molecules--prostanoid receptor-1 or tumour necrosis factor-alpha--might be a viable neuropro

239 Using intravital microscopy of tumour necrosis factor-alpha-challenged mouse cremaster

240 NF)-kappaB activation and protection against tumour necrosis factor-alpha-induced apoptosis.

241 eptor for advanced glycation endproducts and tumour necrosis factor-alpha.

242 with suppression of the circulating level of tumour necrosis factor-alpha.

243 as been shown to induce interferon-gamma and tumour necrosis factor-alpha.

244 imab, a monoclonal antibody directed against tumour necrosis factor-alpha.

245 orming growth factor beta, interleukin-1 and tumour necrosis factor-alpha.

246 clear factor-kappaB and promote synthesis of tumour necrosis factor-alpha.

247 ted therapy, as well as therapies to inhibit tumour necrosis factor-alpha.

248 romoter and cDNA for the gene encoding human tumour necrosis factor-alpha.

249 stimuli and preventing apoptosis induced by tumour necrosis factor-alpha.

250 IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8 and tumour necrosis factor-alpha.

251 and leukocyte adhesion after treatment with tumour necrosis factor-alpha.

252 paracellular permeability induced by H2O2 or tumour necrosis factor-alpha.

253 f cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha; and cell-infiltration, cel

254 miR-21 deletion is also protective in tumour necrosis factor-induced systemic inflammatory res

255 inyl acetate (RAc) independently upregulates tumour necrosis factor-related apoptosis-inducing ligand

256 Tumour necrosis factor-related apoptosis-inducing ligand

257 Tumour necrosis factor-related apoptosis-inducing ligand

258 pression of other receptors for HA, CD44 and tumour necrosis factor-stimulated gene 6 (TSG-6) were ma

259 Tumour necrosis factor-stimulated gene-6 (TSG-6) is a gl

260 and unlike haemorrhagic necrosis induced by tumour necrosis factor.

261 ether A20-deficient cells die in response to tumour necrosis factor.

262 by antibiotic treatment, MYD88 deficiency or tumour-necrosis factor (TNF) receptor 1 deficiency, demo

263 Tumour-necrosis factor (TNF) receptor-associated factor

264 Tumour-necrosis factor (TNF) receptor-associated factor

265 gand engagement of 'death receptors' such as tumour-necrosis factor (TNF) receptor.

266 Excessive inflammation and tumour-necrosis factor (TNF) synthesis cause morbidity a

267 -kappaB nuclear translocation in response to tumour-necrosis factor (TNF), IL-1beta and pathogen-asso

268 (interferon (IFN)-gamma, interleukin (IL)-2, tumour-necrosis factor (TNF)-alpha and lymphotoxin) that

269 tal circulation, leading to enhanced hepatic tumour-necrosis factor (TNF)-alpha expression that drive

270 nt concentrations of the signalling molecule tumour-necrosis factor (TNF)-alpha, and relay informatio

271 This death is mediated by tumour-necrosis factor (TNF)-related apoptosis-inducing

272 Activation of NF-kappaB by tumour-necrosis factor alpha and interleukin-1 was unaff

273 impaired production of interferon-gamma and tumour-necrosis factor by T cells, diminished memory T-c

274 HIES failed to produce IL-17, but not IL-2, tumour-necrosis factor or interferon-gamma, on mitogenic

275 Members of the tumour-necrosis factor receptor (TNFR) family that conta

276 virus entry mediator (HVEM), a member of the tumour-necrosis factor receptor family, has diverse func

277 RE1alpha)-regulated NF-kappaB activation and tumour-necrosis factor signalling, which are synergistic

278 specific approaches, such as the blocking of tumour-necrosis factor, are achieving some success but t

279 a results in a significantly higher level of tumour-necrosis factor-alpha (TNF-alpha) secretion and m

280 ng to production of interleukin-6 (IL-6) and tumour-necrosis factor-alpha (TNF-alpha) through activat

281 is mediated by the pro-inflammatory cytokine tumour-necrosis factor-alpha (TNF-alpha).

282 d key signalling intermediate in the Fas and tumour-necrosis factor-alpha (TNFalpha) death-signalling

283 ecules such as interleukin-4, interleukin-6, tumour-necrosis factor-alpha and granulocyte-macrophage

284 In contrast, secretion of tumour-necrosis factor-alpha and IL-6, as well as activa

285 amma inducing factor) and IFN-gamma, but not tumour-necrosis factor-alpha and IL-6, in response to va

286 he release of the pro-inflammatory cytokines tumour-necrosis factor-alpha and interleukins 6 and 12 i

287 aB by p53 was distinct from that mediated by tumour-necrosis factor-alpha and involved MEK1 and the a

288 , one induced by treatment with the cytokine tumour-necrosis factor-alpha and the other with the gluc

289 nanowires conjugated with a cytokine such as tumour-necrosis factor-alpha can be transported along an

290 atory T-cell induction and inhibiting T-cell tumour-necrosis factor-alpha production through arginase

291 asts are not protected from staurosporine or tumour-necrosis factor-alpha-induced death.

292 F-kappaB-regulated genes on stimulation with tumour-necrosis factor-alpha.

293 -2 blocks the degradation of p105 induced by tumour-necrosis factor-alpha.

294 n has focused on soluble regulators, such as tumour-necrosis factor-alpha.

295 advanced tumours and the upregulation of two tumour-necrosis-factor family members: receptor activato

296 Etanercept, a tumour-necrosis-factor inhibitor, has shown efficacy in

297 ectly lead to cancer development through the tumour-necrosis-factor signalling pathway.

298 empted to induce apoptosis by triggering the tumour-necrosis-factor-related apoptosis-inducing ligand

299 ombinant human apoptosis ligand 2 (Apo2L) or tumour-necrosis-factor-related apoptosis-inducing-ligand

300 inistration (0.05 mg kg(-)(1)) showed higher tumour necrosis using pegylated liposomal formulations i