ライフサイエンスコーパス: tumor necrosis factor

1 s via interleukin 17A, interferon gamma, and tumor necrosis factor.

2 consisted of inflammatory genes, VCAM1, and tumor necrosis factor.

3 of inflammatory monocytes and production of tumor necrosis factor.

4 e an anti-IL-12/23 (ustekinumab, n=50), anti-tumor necrosis factor-a (TNF-alpha; etanercept, n=50), o

5 ifferent trough drug concentrations for anti-tumor necrosis factor agents and thiopurines to inform c

6 er biologics (e.g. vedolizumab) and the anti-tumor necrosis factor agents.

7 No association was found for anti-tumor necrosis factor agents.

8 xpressed interleukin-2 (IL-2) (66.4%) and/or tumor necrosis factor alpha (TNF-alpha) (63.7%).

9 mycobacteria-specific CD4+ T cells secreting tumor necrosis factor alpha (TNF-alpha) but not interfer

10 ng, we find that increases in spine size are tumor necrosis factor alpha (TNF-alpha) dependent and th

11 imidazole-4-carboxamide riboside (AICAR), on tumor necrosis factor alpha (TNF-alpha) induction of com

12 Tumor necrosis factor alpha (TNF-alpha) is a cytokine th

13 ecretion of interferon gamma (IFN)-gamma and tumor necrosis factor alpha (TNF-alpha) that induced tum

14 ncreases in gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) were delayed and

15 hly sensitive biosensor for the detection of tumor necrosis factor alpha (TNF-alpha) within the rando

16 kappaB ligand (RANKL)/osteoprotegerin (OPG), tumor necrosis factor alpha (TNF-alpha), and IL-1beta we

17 on of interleukin 8 (IL-8), CXCL2, IL-1beta, tumor necrosis factor alpha (TNF-alpha), and IL-6.

18 hree cytokines interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin

19 c mice elicits gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin

20 iomarkers, including interleukin (IL) 1beta, tumor necrosis factor alpha (TNF-alpha), CXCL10, CCL5, I

21 ytokines involved in inflammation including: tumor necrosis factor alpha (TNF-alpha), granulocyte mac

22 mune mediators such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interleukin 1be

23 a stimulated the production of the cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-1be

24 cally, the effectors SseK1 and SseK3 inhibit tumor necrosis factor alpha (TNF-alpha)-induced NF-kappa

25 is study, we demonstrate that treatment with tumor necrosis factor alpha (TNF-alpha)-neutralizing ant

26 sets with, gamma interferon (IFN-gamma)- and tumor necrosis factor alpha (TNF-alpha)-producing cells

27 extent similar to that of cells primed with tumor necrosis factor alpha (TNF-alpha).

28 ased renal expression of NF-kappaB-dependent tumor necrosis factor alpha (TNF-alpha).

29 ssue Mvarphi and inhibited the production of tumor necrosis factor alpha (TNF-alpha)/interleukin-6 (I

30 ivation of NF-kappaB signaling and increased tumor necrosis factor alpha (TNFalpha) and inducible nit

31 Plasma levels of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha) are increased in

32 This results in sustained release of soluble tumor necrosis factor alpha (TNFalpha) by ADAM17, which

33 osensor was constructed for the detection of tumor necrosis factor alpha (TNFalpha) by using Poly(3-t

34 Similar results were obtained from tumor necrosis factor alpha (TNFalpha) detection with 3

35 The homotrimeric ligand tumor necrosis factor alpha (TNFalpha) is a key cytokine

36 1/2) activation (i.e. phosphorylation) links tumor necrosis factor alpha (TNFalpha) to pro-inflammato

37 Our previous work demonstrated that tumor necrosis factor alpha (TNFalpha)-activated MSCs si

38 n of a protein-protein interaction involving tumor necrosis factor alpha (TNFalpha).

39 ive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFalpha).

40 ty C-reactive protein, soluble receptors for tumor necrosis factor alpha 1 and 2, the percentages of

41 the miRNAs identified on cytokine secretion (tumor necrosis factor alpha [TNF-alpha] and interleukin-

42 ulated type 1 (gamma interferon [IFN-gamma], tumor necrosis factor alpha [TNF-alpha], and interleukin

43 analyses showed increased expression of A20 (tumor necrosis factor alpha [TNF-alpha]-induced protein

44 or the long-term efficacy and safety of anti-tumor necrosis factor alpha agents (anti-TNF) in treatin

45 tly sensitize PEL to the proapoptotic agents tumor necrosis factor alpha and etoposide and are the fi

46 rotein to the extracellular medium, inducing tumor necrosis factor alpha and interleukin 6 expression

47 I, soluble interleukin-2 receptor alpha, and tumor necrosis factor alpha and lower levels of insulin-

48 pression of IP-DPSCs, whereas treatment with tumor necrosis factor alpha did not.

49 and normalized lipopolysaccharide-stimulated tumor necrosis factor alpha expression in Kupffer cells

50 baboons expressed more gamma interferon and tumor necrosis factor alpha in response to Tax peptides

51 ck of phagocytosis, macrophage production of tumor necrosis factor alpha is triggered by hyphae but n

52 Plasma tumor necrosis factor alpha level was significantly elev

53 Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, is effe

54 rage C-reactive protein (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .

55 h trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05

56 kers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial

57 in 10, hepatocyte growth factor, soluble p75 tumor necrosis factor alpha receptor, vascular cell adhe

58 ta clearly indicated a potent suppression of tumor necrosis factor alpha release.

59 fibroblasts and brown adipose tissues and by tumor necrosis factor alpha that reduces p63 transcripti

60 ities to modulate the biological activity of tumor necrosis factor alpha through stabilization of the

61 natural conformational sampling of the human tumor necrosis factor alpha trimer.

62 duced percentages of CD4+ Th1 (interleukin2, tumor necrosis factor alpha) and Th17 (interleukin 17A)

63 s (eg, interleukin 6, interleukin 1beta, and tumor necrosis factor alpha) in circulating monocytes, p

64 eron, macrophage inflammatory protein 1beta, tumor necrosis factor alpha) was dependent on the peptid

65 f neutrophils fed CA-MRSA was independent of tumor necrosis factor alpha, active RIPK-1, and MLKL, bu

66 IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor necrosis factor alpha, and granulocyte-macrophage

67 ific CD4+ T-cell cytokine (interferon gamma, tumor necrosis factor alpha, and interleukin 2) response

68 e B, granzyme K, perforin, gamma interferon, tumor necrosis factor alpha, and interleukin-2 productio

69 sed and the gingival expression of IL-1beta, tumor necrosis factor alpha, and RANKL was significantly

70 , macrophage inflammatory protein 2, RANTES, tumor necrosis factor alpha, gamma interferon, and inter

71 ctional (ie, they produced interferon gamma, tumor necrosis factor alpha, granulocyte-macrophage colo

72 inent AH patients; however, plasma levels of tumor necrosis factor alpha, IL-8, IL-10, fibroblast gro

73 rum alanine amino transferase, expression of tumor necrosis factor alpha, Il6, interferon mRNA, and l

74 baseline levels of 11 cytokines/chemokines (tumor necrosis factor alpha, interleukin 6 [IL-6], IL-8,

75 lood bacterial density, cytokine production (tumor necrosis factor alpha, interleukin [IL] 6, IL-1bet

76 nfluenza A (H5N1) virus induce expression of tumor necrosis factor alpha, interleukin-6, and interleu

77 ereas infarcts were associated with elevated tumor necrosis factor alpha, macrophage inflammatory pro

78 by Ca2+ depletion, proinflammatory cytokine tumor necrosis factor alpha, or dedifferentiation.

79 In parallel, the proteolytic activity of tumor necrosis factor alpha-converting enzyme (TACE; ADA

80 In addition, TGF-beta1 and BMP-2 antagonized tumor necrosis factor alpha-induced IL-34 gene expressio

81 xt of NASH, we identified the deubiquitinase tumor necrosis factor alpha-induced protein 3 (TNFAIP3)

82 cated at mouse chromosome 10 proximal to the tumor necrosis factor alpha-induced protein 3 (Tnfaip3)

83 matic mutations including Stat3, Stat5b, and tumor necrosis factor alpha-induced protein 3 have been

84 ced proportion of polyfunctional (IFN-gamma+/tumor necrosis factor alpha-positive) CD4+ and CD8+ T ce

85 uced expression of proinflammatory mediators tumor necrosis factor-alpha (P = 0.04) and inducible nit

86 03) and LPS-stimulated ex vivo production of tumor necrosis factor-alpha (P = 0.04) in the WG group t

87 e CRP (SMD: -0.40; 95% CI: -0.73, -0.06) and tumor necrosis factor-alpha (SMD -0.90; 95% CI: -1.50, -

88 Anti-tumor necrosis factor-alpha (TNF) antibodies are mainsta

89 atients respond selectively to inhibitors of tumor necrosis factor-alpha (TNF).

90 of the pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) and interleukin-

91 equivalence between biosimilar and reference tumor necrosis factor-alpha (TNF-alpha) inhibitors.

92 sforming growth factor-beta1 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha) play key roles i

93 aB) activity, resulting in downregulation of tumor necrosis factor-alpha (TNF-alpha) production and c

94 Tumor necrosis factor-alpha (TNF-alpha) stimulation can

95 hippocampal interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were assessed.

96 panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)), were analyzed

97 hs-CRP), interleukin-1beta (IL-1beta), IL-6, tumor necrosis factor-alpha (TNF-alpha), and chemokine (

98 els of angiopoietin-2, interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and vascular en

99 xpressed in Muller cells upregulated retinal tumor necrosis factor-alpha (TNF-alpha), interleukin 1be

100 ncubated with interferon-gamma (IFNgamma) or tumor necrosis factor-alpha (TNF-alpha), or co-cultured

101 o platelet-derived growth factor (PDGF)- and tumor necrosis factor-alpha (TNF-alpha)-induced vascular

102 kinase (p38 MAPK) activation and release of tumor necrosis factor-alpha (TNF-alpha).

103 d molecular cascades of initial increases in tumor necrosis factor-alpha (TNFalpha) and interleukin (

104 of varying stiffness and treated with either tumor necrosis factor-alpha (TNFalpha) or thrombin.

105 B cells, which produced elevated amounts of tumor necrosis factor-alpha (TNFalpha) that contributed

106 oncentrations both cytokines synergized with tumor necrosis factor-alpha (TNFalpha) to increase recru

107 ride (LPS)-induced human monocyte release of tumor necrosis factor-alpha (TNFalpha) was assessed by E

108 ne expression (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and IL-6) by qu

109 TDM for biologic therapy, specifically anti-tumor necrosis factor-alpha agents, and for thiopurines.

110 Third, expression of tumor necrosis factor-alpha and amyloid A mRNA levels in

111 CC chemokine ligand 20 induction by tumor necrosis factor-alpha and IL-17A was reduced in Tr

112 , whereas CC chemokine ligand 5 induction by tumor necrosis factor-alpha and IL-4 was enhanced.

113 st cancer survivors had significantly higher tumor necrosis factor-alpha and IL-6 compared with the c

114 ression of proinflammatory cytokines such as tumor necrosis factor-alpha and IL-6.

115 Treatment of Caco-2 cells with tumor necrosis factor-alpha and interferon-gamma signifi

116 Ns also significantly reduced the release of tumor necrosis factor-alpha and interleukin-1 beta, whic

117 iated with plasma cytokine levels, including tumor necrosis factor-alpha and interleukin-6 at baselin

118 anti-inflammatory effects of OxPAPC against tumor necrosis factor-alpha and lipopolysaccharide chall

119 Tumor necrosis factor-alpha and, to a lesser extent, IL-

120 , multicenter study evaluated the effects of tumor necrosis factor-alpha antagonist adalimumab on vas

121 ular inflammation in patients treated with a tumor necrosis factor-alpha antagonist or placebo and a

122 d rheumatoid arthritis patients treated with tumor necrosis factor-alpha antagonists.

123 and larger studies are needed to explain why tumor necrosis factor-alpha blockade appears to reduce c

124 Tumor necrosis factor-alpha blockade is the treatment of

125 Tumor necrosis factor-alpha decreased (p = 0.0001 for ea

126 Furthermore, tumor necrosis factor-alpha decreased both mineralocorti

127 nduced release of the proinflammatory marker tumor necrosis factor-alpha in blood displayed a reducti

128 enocorticotropic hormone, interleukin-6, and tumor necrosis factor-alpha in mice exposed to chronic m

129 e expression of the proinflammatory cytokine tumor necrosis factor-alpha in microglia, and the recrui

130 Moreover, the increased level of tumor necrosis factor-alpha in those cerebrospinal fluid

131 d anti-inflammatory effect of OxPAPC against tumor necrosis factor-alpha in vitro and in the animal m

132 Tumor necrosis factor-alpha induced extrinsic apoptosis

133 -4, IL-5, IL-7, IL-17, interferon-gamma, and tumor necrosis factor-alpha levels were higher in C-IRIS

134 AAT-treated mice showed reduced serum tumor necrosis factor-alpha levels, decreased lymphocyti

135 human antigen R (HuR) RNA-binding protein to tumor necrosis factor-alpha mRNA.

136 Levels of interleukin-8 and tumor necrosis factor-alpha produced by neutrophils were

137 ell death compared with wild-type cells, and tumor necrosis factor-alpha release was completely block

138 terleukin (IL)-1beta, IL-4, IL-6, IL-17, and tumor necrosis factor-alpha using an assay system.

139 Tumor necrosis factor-alpha was identified as a key proi

140 A diabetic retinopathy (DR) biomarker, tumor necrosis factor-alpha was selected to evaluate the

141 thermore, TRX80 was found to colocalize with tumor necrosis factor-alpha, a macrophage M1 marker, in

142 wed increased expression of interferon-beta, tumor necrosis factor-alpha, and CXCL1, induced oxidativ

143 timulated production of interleukin [IL] -6, tumor necrosis factor-alpha, and IL-1beta).

144 y proteins (inducible nitric oxide synthase, tumor necrosis factor-alpha, and interleukin 6).

145 NA expression of AT1R, IL-1beta, IL-6, IL-8, tumor necrosis factor-alpha, and osteoprotegerin (OPG) i

146 , IL-10, monocyte chemoattractant protein-1, tumor necrosis factor-alpha, C-reactive protein, and pho

147 erleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, tumor necrosis factor-alpha, epidermal growth factor, IL

148 This dataset showed tumor necrosis factor-alpha, IFN-gamma, transforming gro

149 acute pancreatitis patients, including IL-6, tumor necrosis factor-alpha, IL-1beta, chemokine (C-C mo

150 d levels of cytokines and chemokines such as tumor necrosis factor-alpha, interferon-gamma, interleuk

151 t of ligature induced significantly elevated tumor necrosis factor-alpha, interleukin-1beta, and RANK

152 Serum tumor necrosis factor-alpha, interleukins, hemogram, and

153 ding to influenza A virus (A/WSN/33 [H1N1]), tumor necrosis factor-alpha, LPS, mechanical stretch/ven

154 showed that ECs treated with M1 macrophages, tumor necrosis factor-alpha, or IL-1beta decreased the e

155 tively), matrix metalloproteinase-9 (MMP-9), tumor necrosis factor-alpha, plasminogen activator inhib

156 LPS transiently increased interleukin-6 and tumor necrosis factor-alpha, sickness symptoms, body tem

157 elevated levels of CB1R, interleukin-1beta, tumor necrosis factor-alpha, the chemokine CCL2, and int

158 opsy led to the targeted treatment with anti-tumor necrosis factor-alpha, which was highly effective

159 contrast, the matrix metalloproteinase/TACE (tumor necrosis factor-alpha-converting enzyme) inhibitor

160 of activated B cells and negative regulators tumor necrosis factor-alpha-induced protein 3 (A20) and

161 We find that tumor necrosis factor-alpha-stimulated neutrophil adhere

162 se activation and upregulation of CXCL10 and tumor necrosis factor-alpha.

163 IL)-1beta, IL-6, keratinocyte chemokine, and tumor necrosis factor-alpha.

164 After stimulation of ECs with tumor-necrosis factor-alpha (TNF-alpha) the supernatants

165 (controls) exposed to cell stressors such as tumor necrosis factor and adherent-invasive Escherichia

166 s showed increased release of IL-10, whereas tumor necrosis factor and cathepsin L release was reduce

167 as significantly greater expression of human tumor necrosis factor and interleukin 6 (84% and 51% res

168 virus-induced proinflammatory cytokines like tumor necrosis factor and interleukin-1.

169 drome characterized by the overexpression of tumor necrosis factor and other inflammatory mediators.

170 ed genes in liver metastases showed aberrant tumor necrosis factor and transforming growth factor sig

171 (60%), biological therapy (66%, mostly anti-tumor necrosis factor) and phototherapy (15%) (P < .001)

172 T cells and expression of interferon-gamma, tumor necrosis factor, and EOMES.

173 activator of transcription 3, interleukin-6, tumor necrosis factor, and forkhead box P3 prominently p

174 ion of proinflammatory genes for IL-6, IL-8, tumor necrosis factor, and IL-1B, whereas keratinocytes

175 ants had significantly higher levels of CRP, tumor necrosis factor, and interleukin 6 and shorter leu

176 vious conventional therapy or therapy with a tumor necrosis factor antagonist were randomly assigned

177 rohn's disease who had failed treatment with tumor necrosis factor antagonists, 8 and 24 weeks of tre

178 derate to severe CD failed by treatment with tumor necrosis factor antagonists.

179 sion at day 1 with an associated decrease in tumor necrosis factor-beta, interferon-gamma, and monocy

180 ttributed to the anti-inflammatory effect of tumor necrosis factor blockers, but a 52-week study cond

181 ammatory markers including interferon gamma, tumor necrosis factor, CXCL13, and CXCL10 with leniolisi

182 APRIL is a member of the tumor necrosis factor cytokine family involved in the re

183 : exogenous CCL3 rescues the OM phenotype of tumor necrosis factor-deficient mice and the function of

184 including the long-sought-after nephrin and tumor necrosis factor genes.

185 sease under induction of the inducible human tumor necrosis factor (hTNF) transgene than wild-type mi

186 f the M1-associated proinflammatory cytokine tumor necrosis factor, inducible nitric oxide synthase,

187 Medication-related AEs occur less often with tumor necrosis factor inhibitors than with methotrexate.

188 halidomide, cyclophosphamide, hemoperfusion, tumor necrosis factor inhibitors, and granulocyte colony

189 d in 20 of 106 patients (18.9%) treated with tumor necrosis factor inhibitors, but did not lead to di

190 drug was more likely with methotrexate than tumor necrosis factor inhibitors, but having 1 or more i

191 Monocytes that produce tumor necrosis factor interact with cerebral endothelial

192 with high levels of inflammatory cytokines: tumor necrosis factor, interleukin (IL)-6, and reactive

193 ociated with serum C-reactive protein (CRP), tumor necrosis factor, interleukin 1beta, 6, and 10, leu

194 ur pathophysiologic domains: "inflammation" (tumor necrosis factor, interleukin-6, and -10); "coagula

195 The precise mechanism by which binding of tumor necrosis factor ligands to the extracellular domai

196 Ectodysplasin (Eda), a tumor necrosis factor-like ligand, is essential for the

197 Similarly, orally given LPA blocked tumor necrosis factor-mediated intestinal barrier defect

198 by cardiac restricted overexpression of TNF (tumor necrosis factor; Myh6-sTNF).

199 nduced by death receptors ligands TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related Apoptosis-I

200 by the upregulation of both interferon- and tumor necrosis factor-positive CD4(+) T cells and CD8(+)

201 (nuclear factor-kappaB) activation and TNF (tumor necrosis factor) production by myeloid cells.

202 rating oxygenation index, interleukin-8, and tumor necrosis factor-R2 was superior to a model of oxyg

203 eukin-8, interleukin-10, interleukin-18, and tumor necrosis factor-R2 were each strongly associated w

204 deletion of GATA3, and mice with deletion of tumor necrosis factor receptor (TNFR) 1 and TNFR2 (TNFR

205 The interaction of the tumor necrosis factor receptor (TNFR) CD27 with its liga

206 0 (1.35), fatty acid-binding protein (1.33), tumor necrosis factor receptor 1 (2.29), and TNF-related

207 Activation of the tumor necrosis factor receptor 1 (TNFR1) death receptor

208 We hypothesized that tumor necrosis factor receptor 1 (TNFR1) levels are asso

209 ptor (TCR) or from a death receptor, such as tumor necrosis factor receptor 1 (TNFR1) or Fas.

210 e signaling and cell death pathways, notably tumor necrosis factor receptor 1 (TNFR1) signaling.

211 Tumor necrosis factor receptor 1, E-selectin, hK11, tumo

212 Tumor necrosis factor receptor 2 (TNFR2) is known to med

213 ulating CD4+CD25+CD127lo/- and CD4+CD127lo/- tumor necrosis factor receptor 2 (TNFR2)+ Treg cells wer

214 Wild-type C57Bl/6 mice or tumor necrosis factor receptor 2 knockout mice, either f

215 Blockade, by either monoclonal antibody or tumor necrosis factor receptor gene knockout, reduced in

216 the role of neuronally expressed, paralogous tumor necrosis factor receptor super family (TNFRSF) mem

217 4-1BB (CD137, tumor necrosis factor receptor superfamily 9) is an indu

218 cell precursors expressed high levels of the tumor necrosis factor receptor superfamily molecule GITR

219 olecules to mediate signal transduction from Tumor Necrosis Factor Receptor to downstream effector mo

220 ree-variable model of IL-8, bicarbonate, and tumor necrosis factor receptor-1 accurately classified t

221 ietin-1, angiopoietin-2, IL-6, IL-8, soluble tumor necrosis factor receptor-1, soluble vascular cell

222 We examined the role of tumor necrosis factor receptor-associated factor 2 (Traf

223 The tumor necrosis factor receptor-associated factor 2 (TRAF

224 eus to mitochondria, where it interacts with tumor necrosis factor receptor-associated factor 2 (TRAF

225 m specifically induces the ubiquitination of tumor necrosis factor receptor-associated factor 6 (TRAF

226 1 and M2 subsets was critically dependent on tumor necrosis factor receptor-associated factor 6 (TRAF

227 d low levels of Cathepsin K, TRAP, RANK, and tumor necrosis factor receptor-associated factor 6 mRNAs

228 e receptors, IL-1 receptor-associated kinase/tumor necrosis factor receptor-associated factor-6, IL8/

229 croptotic signaling with the adaptor protein tumor necrosis factor receptor-associated protein with d

230 motif, IProx, that shares homology with the tumor-necrosis-factor receptor (TNFR)-associated factors

231 ies have proposed that activation of several tumor necrosis factor receptors, including Death Recepto

232 S163R) in the C1QTNF5 gene, encoding C1q And Tumor Necrosis Factor Related Protein 5 (C1QTNF5) has be

233 ecrosis factor receptor 1, E-selectin, hK11, tumor necrosis factor-related activation-induced cytokin

234 While tumor necrosis factor-related apoptosis inducing ligand

235 tosis by up-regulation of gene expression of tumor necrosis factor-related apoptosis-inducing ligand

236 ty in individual cells following exposure to tumor necrosis factor-related apoptosis-inducing ligand

237 otype, and assists TRXR1-regulated arrest of tumor necrosis factor-related apoptosis-inducing ligand-

238 ntified C1QTNF2, encoding for Complement C1q tumor necrosis factor-related protein 2, a secreted adip

239 Tumor necrosis factor-stimulated enhanced expression and

240 tor-kappaB ligand and increased osteoblastic tumor necrosis factor superfamily member 11 (Tnfsf11) ex

241 in-10 (IP-10), interferon gamma (IFN-gamma), tumor necrosis factor superfamily member 14 (TNFSF14, al

242 BACKGROUND & AIMS: Variants in the tumor necrosis factor superfamily member 15 gene (TNFSF1

243 s the strongest in those initiated with anti-tumor necrosis factor therapy (beta = 0.79; 95% CI, 0.26

244 to characterize the impact of 1 year of anti-tumor necrosis factor therapy on vascular inflammation.

245 Interestingly, the transmembrane form of tumor necrosis factor (tmTNF) is necessary to robustly a

246 The risk of lymphoma associated with anti-tumor necrosis factor (TNF) agents either alone or in co

247 easles had higher levels of innate cytokines tumor necrosis factor (TNF) alpha, interleukin 1beta (IL

248 increased release of interleukin (IL) 6 and tumor necrosis factor (TNF) alpha.

249 ignaling networks, binding ligands from both tumor necrosis factor (TNF) and immunoglobulin (Ig) supe

250 deficient P. aeruginosa had higher levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6), mo

251 Tumor necrosis factor (TNF) and its receptors are up-reg

252 BACKGROUND & AIMS: Although tumor necrosis factor (TNF) antagonists reduce many clin

253 e hypothesis that interleukin 17 (IL-17) and tumor necrosis factor (TNF) are key cytokines involved i

254 VLX103 decreased GalN/LPS induction of tumor necrosis factor (TNF) but had no effect on other p

255 recovery of barrier function in response to tumor necrosis factor (TNF) compared with normal donor E

256 The tumor necrosis factor (TNF) family ligand ectodysplasin

257 reactive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupffer cells caused JN

258 Tumor necrosis factor (TNF) has a critical role in diver

259 he peptide substance P (SP) and the cytokine tumor necrosis factor (TNF) have been implicated in infl

260 had previously had an inadequate response to tumor necrosis factor (TNF) inhibitors.

261 BACKGROUND AND AIMS: Tumor necrosis factor (TNF) is a cytokine that promotes

262 BACKGROUND & AIMS: Tumor necrosis factor (TNF) is an inflammatory cytokine

263 Tumor necrosis factor (TNF) is best known for inducing a

264 Some mice were given siRNA against tumor necrosis factor (Tnf) mRNA for 6 days; colon tissu

265 Dysregulation of tumor necrosis factor (TNF) receptor signaling is a key

266 rapid adaptive response driven by increased tumor necrosis factor (TNF) secretion, which leads to ac

267 Analysis of tumor necrosis factor (TNF) signaling pathway which regu

268 stem, we show that synergistic IFN-gamma and tumor necrosis factor (TNF) stimulation promotes strong

269 that in the absence of Eiger, the only known tumor necrosis factor (TNF) superfamily homolog in Droso

270 CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily, binds to CD40,

271 Despite the increasing use of anti-tumor necrosis factor (TNF) therapy in ulcerative coliti

272 Tumor necrosis factor (TNF), a product of TLR4 signaling

273 proinflammatory innate cytokines, including tumor necrosis factor (TNF), IL-6, IL-12, IL-23, and IL-

274 nzyme-linked immunosorbent assays quantified tumor necrosis factor (TNF), interleukin (IL)-12, and IL

275 sma levels of inflammatory cytokines such as tumor necrosis factor (TNF), interleukin 1beta (IL-1beta

276 lammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor (TNF), leading to activation of si

277 R, PPARG coactivator 1 alpha (PPARGC1A), and tumor necrosis factor (TNF), was changed in adipose tiss

278 ization and osteoclastogenesis by modulating tumor necrosis factor (TNF)-alpha and -beta.

279 matory diseases marked by elevated levels of tumor necrosis factor (TNF)-alpha and IL-17A, pathologic

280 levels and decreased interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and IL-1beta protein l

281 zed by production of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-2

282 Monoclonal antibodies directed against tumor necrosis factor (TNF)-alpha have been studied most

283 cular endothelial growth factor (VEGF-A) and tumor necrosis factor (TNF)-alpha levels.

284 Cytokine interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha produced by NK cells a

285 luid (GCF) levels of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and high-sensitive C-

286 ulation and in NCM460 cells after IL-6, IL8, tumor necrosis factor (TNF)-alpha, and interferon-gamma

287 stologic effects of P4 and the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1bet

288 s-vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1bet

289 and salivary markers interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, nitric oxide (NO), an

290 , including IL-1alpha, IL-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, the proangiogenic and

291 g-related dendritic spine plasticity through tumor necrosis factor (TNF)-alpha-dependent mechanisms.

292 ifferentiation primary response gene-88, and tumor necrosis factor (TNF)-alpha.

293 In tumor necrosis factor (TNF)-deficient mice, which are pr

294 inducible nitric oxide synthase (NOS2)- and tumor necrosis factor (TNF)-producing dendritic cells (D

295 Tumor necrosis factor (TNF)-related apoptosis-inducing l

296 easing that of the pro-inflammatory cytokine tumor necrosis factor (TNF).

297 levels of inflammatory cytokines, including tumor necrosis factor (TNF).

298 erleukin 6 receptor [sIL-6R], soluble gp130, tumor necrosis factor [TNF]), enterocyte turnover (intes

299 markers (CD107, CD154, interleukin-2 [IL-2], tumor necrosis factor [TNF], and IFN-gamma) and memory p

300 TRX-1 and LPS-stimulated hyperproduction of tumor-necrosis-factor-(TNF)-alpha by monocytes and neutr