ライフサイエンスコーパス: tumour necrosis

1 to pyroptosis in cancer cells, resulting in tumour necrosis.

2 pyroptosis pathway in cancer cells, causing tumour necrosis.

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

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

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

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

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

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

9 es, including biologics (in particular, anti-tumour necrosis factor (TNF) agents).

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

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

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

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

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

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

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

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

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

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

20 Tumour necrosis factor (TNF) is a cytokine belonging to

21 Tumour necrosis factor (TNF) is a key cytokine during in

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

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

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

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

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

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

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

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

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

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

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

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

34 Since the early 2000s, anti-tumour necrosis factor (TNF) treatment has significantly

35 on of death receptor family ligands, such as tumour necrosis factor (TNF), can sensitize cells in the

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

37 We show that tumour necrosis factor (TNF), IFNgamma, and glutamate ca

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

39 Tumour necrosis factor (TNF), like TLR3 or TLR4 agonists

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

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

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

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

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

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

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

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

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

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

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

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

52 les that control the interferon response and tumour necrosis factor (TNF)-induced cytotoxicity are do

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

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

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

56 of hepcidin expression by BMP6, probably via tumour necrosis factor (TNF)-mediated downregulation of

57 entified death receptor 5 (DR5), a member of tumour necrosis factor (TNF)-receptor superfamily, as a

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

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

60 1beta, IL-1 receptor antagonist (IL-1ra) and tumour necrosis factor (TNF).

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

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

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

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

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

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

67 ) and inflammatory cytokines and chemokines (tumour necrosis factor [Tnf], Il1b, Ccl3/4) indicated th

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

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

70 50, p<0.0001), C5a (48%, n=41, p=0.0005), or tumour necrosis factor alpha (52%, n=27, p<0.0001).

71 fection is routine before initiation of anti-tumour necrosis factor alpha (anti-TNFalpha) agents in t

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

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

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

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

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

77 were exposed to increasing concentrations of tumour necrosis factor alpha (TNF-alpha) or lipopolysacc

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

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

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

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

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

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

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

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

86 ded production of a gene product, namely the tumour necrosis factor alpha (TNFalpha) cytokine.

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

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

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

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

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

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

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

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

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

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

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

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

99 d by reductions in plasma and adipose tissue tumour necrosis factor alpha and interleukin 6 concentra

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

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

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

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

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

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

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

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

108 Tumour necrosis factor alpha receptor 1 (TNFR1) activati

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

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

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

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

113 Tumour necrosis factor alpha, vascular cell adhesion mol

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

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

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

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

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

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

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

121 verall, we found that host-derived cytokines tumour necrosis factor and interleukin-1alpha stimulated

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

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

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

125 rise antibiotic treatment, neutralization of tumour necrosis factor and surgical intervention togethe

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

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

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

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

130 Anti-tumour necrosis factor drugs were most commonly studied

131 Tumour necrosis factor exists in two biologically active

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

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

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

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

136 sation was stratified by weight and previous tumour necrosis factor inhibitor exposure.

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

138 Tumour necrosis factor inhibitors (TNFi) and other biolo

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

140 Tumour necrosis factor inhibitors were the first biologi

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

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

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

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

145 Tumour necrosis factor is linked to the pathophysiology

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

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

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

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

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

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

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

153 terleukin-6 (IL-6) (0.429, p<0.005), soluble tumour necrosis factor receptor 1 (sTNFR1) (0.763, p<0.0

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

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

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

157 This event expels tumour necrosis factor receptor 1 into the disordered li

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

159 receptor 1 (sTNFR1) (0.763, p<0.05), soluble tumour necrosis factor receptor 2 (sTNFR2) (0.354, p<0.0

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

161 on agents directed at members of the CD28 or tumour necrosis factor receptor families.

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

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

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

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

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

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

168 o-creatinine ratio (uACR) and plasma soluble tumour necrosis factor receptor-1 (sTNFR1) with respect

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

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

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

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

173 Multiple members of the tumour necrosis factor superfamily (TNFSF) regulate the

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

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

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

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

178 e reveal an unexpected link between the TNF (tumour necrosis factor) inflammatory pathway, triggered

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

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

181 roles for pro-inflammatory cytokines such as tumour necrosis factor, IL-1beta and IL-17.

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

183 Tumour necrosis factor, which suppresses the generation

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

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

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

187 ke growth factor-1 (P < 0.01) and ~60% lower tumour necrosis factor-alpha (P < 0.05).

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

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

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

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

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

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

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

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

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

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

198 model of RA and assessed for the role of the tumour necrosis factor-alpha (TNF-alpha) inhibitor Infli

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

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

201 APAP and carbon tetrachloride) by increasing tumour necrosis factor-alpha (TNF-alpha) production whic

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

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

204 ctivity of the Rab3 and Rab27 small GTPases, tumour necrosis factor-alpha (TNF-alpha)-induced signall

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

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

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

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

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

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

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

212 ies have shown an association between use of tumour necrosis factor-alpha (TNFalpha) inhibitors and i

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

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

215 Safety of anti-tumour necrosis factor-alpha (TNFalpha) therapy in peopl

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

217 -2, prostaglandin E2, prostanoid receptor-1, tumour necrosis factor-alpha and interleukin-1beta were

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

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

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

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

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

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

224 While tumour necrosis factor-alpha contributes to inflammation

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

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

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

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

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

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

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

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

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

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

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

236 ow inducible nitric oxide synthase and lower tumour necrosis factor-alpha), pro-healing immune profil

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

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

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

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

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

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

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

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

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

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

247 -10, interleukin-12p40, interferon-gamma and tumour necrosis factor-alpha.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 Tumour necrosis factor-related apoptosis-inducing ligand

263 Tumour necrosis factor-related apoptosis-inducing ligand

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

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

266 and unlike haemorrhagic necrosis induced by tumour necrosis factor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

299 ired for macrophage-derived TNFalpha-induced tumour necrosis in vivo.

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