ライフサイエンスコーパス: tumor necrosis factor-alpha

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

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

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

4 13.4% +/- 7.0%, respectively; P = 0.86), and tumor necrosis factor-alpha (-14.8% +/- 5.1% compared wi

5 erferon gamma (6.79% vs 3.20%; P = .017) and tumor necrosis factor alpha (6.98% vs 2.96%; P = .012),

6 terleukin 6: 38% +/- 24% increase; P < 0.05; tumor necrosis factor alpha: 64% +/- 24% increase; P < 0

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

8 Tumor necrosis factor-alpha activates RelA, propagating

9 n necroptosis, which occurs independently of tumor necrosis factor alpha activation.

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

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

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

13 , IL-6, transforming growth factor-beta, and tumor necrosis factor-alpha, along with STAT3 and miR-21

14 protein 9) and an age-dependent increase in tumor necrosis factor-alpha, an activator of ADAM9, thes

15 ined by increased levels of soluble CD14 and tumor necrosis factor alpha and by the presence of CD38(

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

17 wlesi alone failed to develop mitogen-driven tumor necrosis factor alpha and IL-10, indicating the in

18 tic epitope-specific CD8(+) T cells produced tumor necrosis factor alpha and interleukin 2 at the int

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

20 -) and inflammatory monocytes, production of tumor necrosis factor alpha and interleukin 6, as measur

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

22 on of prominent osteoclast-promoting factors tumor necrosis factor alpha and M-CSF was increased by B

23 +) T cells that coproduced interleukin 2 and tumor necrosis factor alpha and were associated with pro

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

25 ent with elamipretide also normalized plasma tumor necrosis factor-alpha and C-reactive protein and r

26 rophil accumulation and the plasma levels of tumor necrosis factor-alpha and granulocyte macrophage c

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

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

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

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

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

32 minotransferase and liver mRNA expression of tumor necrosis factor-alpha and interleukin 1beta and im

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

34 cellular signal-regulated kinase, as well as tumor necrosis factor-alpha and interleukin-1beta, were

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

36 adipocyte-specific hRBP4 mice have increased tumor necrosis factor-alpha and leptin expression and cr

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

38 In vitro, tumor necrosis factor-alpha and lipopolysaccharide direc

39 ive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha and the systemic inflammator

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

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

42 mmatory cytokines (such as interleukin-1 and tumor necrosis factor-alpha) and chemokines (such as mon

43 ubiquitous type 6-phosphofructo-2-kinase and tumor necrosis factor-alpha) and increases (18)F-FDG upt

44 olam plasma (n = 532), cytokine (e.g., IL-6, tumor necrosis factor-alpha), and C-reactive protein (CR

45 interleukin 2, 6, and 10, interferon gamma, tumor necrosis factor alpha, and C-reactive protein than

46 tivation, owing to their capacity to produce tumor necrosis factor alpha, and exhibit greater resista

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

48 -1beta, interleukin 6 (IL-6), interleukin 8, tumor necrosis factor alpha, and interleukin 10 (IL-10)

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

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

51 on levels of soluble RANKL, osteoprotegerin, tumor necrosis factor alpha, and M-CSF in cultured BMSCs

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

53 ising granulocyte colony-stimulating factor, tumor necrosis factor alpha, and several regulatory cyto

54 ma n-terminal pro-brain natriuretic peptide, tumor necrosis factor-alpha, and C-reactive protein were

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

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

57 ssion of proinflammatory cytokines IL-1beta, tumor necrosis factor-alpha, and IL-6 in ONFH compared w

58 inflammation such as CRP, interleukin-6, and tumor necrosis factor-alpha, and inflammation markers we

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

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

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

62 otent suppressor of IL-1beta-induced MMP-13, tumor necrosis factor-alpha, and other catabolic marker

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

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

65 edian age, 42 years [20-55 years] treated by tumor necrosis factor-alpha antagonists [80%] or tociliz

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

67 ponsive to treatment with antibodies against tumor necrosis factor-alpha (anti-TNF-alpha), the most e

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

69 Tumor necrosis factor-alpha blockade is the treatment of

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

71 ory signature with an increased secretion of tumor necrosis factor-alpha, chemokine (C-C motif) ligan

72 Molecular studies revealed that hypoxia and tumor necrosis factor-alpha, conditions accompanying AMI

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

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

75 During KET, serum tumor necrosis factor-alpha, cortisol, glucagon, and gro

76 ith increased ocular media concentrations of tumor necrosis factor-alpha, CXCL1, IL-6, IL-5, chemokin

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

78 Furthermore, tumor necrosis factor-alpha decreased both mineralocorti

79 B kinase) inhibitor BI605906 both inhibited tumor necrosis factor-alpha-dependent IkappaB degradatio

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

81 sion, revealed the presence of IFN-gamma and tumor necrosis factor alpha during early and late immuno

82 03-4.71] p < 0.0001) and decreased levels of tumor necrosis factor-alpha, E selectin, and P selectin,

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

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

85 of microglia and induces profound release of tumor necrosis factor alpha from microglia via activatio

86 38.6 +/- 0.5 degrees C (p < 0.01) and plasma tumor necrosis factor-alpha from 6 pg/mL (3-8 pg/mL) to

87 rkers of exhaustion, and (iii) produced less tumor necrosis factor alpha, gamma interferon, and granz

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

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

90 ailure of these novel therapies such as anti-tumor necrosis factor-alpha has resulted in further comp

91 back circuit on BMP signaling, involving the tumor necrosis factor alpha homolog eiger.

92 ated with S100A8/A9 secrete IL-6, CXCL1, and tumor necrosis factor alpha; however, Mrp14(-/-) cells e

93 latently HIV-1-infected J89 cells with human tumor necrosis factor alpha (hTNF-alpha)/romidepsin (RMD

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

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

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

97 xpression in KCs stimulated the secretion of tumor necrosis factor-alpha, IL-1beta, IL-6, IL-8, and m

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

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

100 ase of interleukin-6, interleukin-1beta, and tumor necrosis factor-alpha in adrenal protein extracts

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

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

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

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

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

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

107 Tumor necrosis factor-alpha induced extrinsic apoptosis

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

109 We found the promoter of tumor necrosis factor alpha-induced protein 2 (TNFAIP2)

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

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

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

113 ration required to achieve 30% inhibition of tumor necrosis factor-alpha-induced CXCL8 production in

114 mouse cremaster microcirculation showed that tumor necrosis factor-alpha-induced endothelial NP/GC-A/

115 se), C242T p22(phox) significantly inhibited tumor necrosis factor-alpha-induced Nox2 maturation, O2

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

117 Mean plasma levels of tumor necrosis factor alpha, interferon gamma, and inter

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

119 ive effector functions (i.e., interleukin-2, tumor necrosis factor-alpha, interferon-gamma, perforin,

120 Tumor necrosis factor alpha, interleukin 10, and the exp

121 dless of anti-HBs level, tested positive for tumor necrosis factor alpha, interleukin 10, or interleu

122 mmatory markers, including interferon gamma, tumor necrosis factor alpha, interleukin 1beta, interleu

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

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

125 levels of interleukin-1beta, interleukin-6, tumor necrosis factor alpha, interleukin-10, and interfe

126 , RANTES, macrophage inflammatory protein 2, tumor necrosis factor alpha, interleukin-1beta, inducibl

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

128 uncture-mediated up-regulation of cytokines (tumor necrosis factor-alpha, interleukin-1beta) and rest

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

130 es in circulating proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, interleu

131 54), type 1 T helper-(CD195/interferon-gamma/tumor necrosis factor-alpha/interleukin-2), and prolifer

132 matory and pronociceptive mediators, such as tumor necrosis factor alpha, interleukins 1beta and 18,

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

134 e in the levels of antiangiogenic (TNFalpha [tumor necrosis factor alpha], IP-10 [interferon gamma-in

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

136 Plasma tumor necrosis factor alpha level was significantly elev

137 The PDE4B inhibitor reduced tumor necrosis factor-alpha levels and increased phospho

138 rleukin-6, C-reactive protein, resistin, and tumor necrosis factor-alpha levels by 3-29%.

139 In our model, serum tumor necrosis factor-alpha levels progressively increas

140 -4, IL-5, IL-7, IL-17, interferon-gamma, and tumor necrosis factor-alpha levels were higher in C-IRIS

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

142 /- 4.73 pmol/minute/mg protein; P <0.05); 2) tumor necrosis factor alpha (LPS: 185.70 +/- 25.63 pg/mg

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

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

145 Hypoxia and cytokines, such as tumor necrosis factor-alpha, modify the endothelial post

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

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

148 s interleukin-6 production without affecting tumor necrosis factor-alpha, nitric oxide, and interleuk

149 ttenuated by neutralizing antibodies against tumor necrosis factor-alpha or after silencing or inhibi

150 al Nox2 activation and oxidative response to tumor necrosis factor-alpha or high-glucose stimulation.

151 When cells were stimulated with tumor necrosis factor-alpha (or high glucose), C242T p22

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

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

154 CD4(+) T cells coproducing interleukin-2 and tumor necrosis factor alpha (P = .003), which were assoc

155 rment at 1 month; SDF1-alpha (P = 0.004) and tumor necrosis factor alpha (P = 0.006) were independent

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

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

158 rs; increased interleukin-1beta (P = 0.004), tumor necrosis factor-alpha (P = 0.040), and interferon-

159 worse shock, systemic inflammation (elevated tumor necrosis factor-alpha, p = 0.003; interleukin-6, p

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

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

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

163 7(-/low) cells, which efficiently suppressed tumor necrosis factor alpha production by the total PBMC

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

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

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

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

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

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

170 autocrine feedback of interleukin 1beta and tumor necrosis factor alpha released from infected macro

171 After adjustment for multiple comparisons, tumor necrosis factor alpha remained significantly highe

172 deactivation (reduced HLA-DR expression and tumor necrosis factor alpha response to lipopolysacchari

173 nza vaccine also showed greater expansion of tumor necrosis factor alpha-secreting CD8(+)CD69(+) T ce

174 elper type 1-prone (ie, interferon gamma- or tumor necrosis factor alpha-secreting) CD4(+) T cell res

175 ed Aspergillus-induced interleukin 1beta and tumor necrosis factor alpha secretion by PBMCs.

176 ase 2 trial, adalimumab, an antibody against tumor necrosis factor alpha, showed efficacy against hid

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

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

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

180 egrity, but neither of them was dependent on tumor necrosis factor alpha stimulation.

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

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

183 y cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha, thereby contributing to hep

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

185 Transmembrane tumor necrosis factor-alpha (tmTNF-alpha) is the prime l

186 gamma (IFN-gamma(+))/interleukin 2 (IL-2(+))/tumor necrosis factor alpha (TNF-alpha(+)) CD4(+) T-cell

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

188 -deficient mice have increased production of tumor necrosis factor alpha (TNF-alpha) and IL-1beta com

189 e presence of two proinflammatory cytokines, tumor necrosis factor alpha (TNF-alpha) and interleukin-

190 e TLR4 pathway, leading to the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-

191 ts to which they influenced the secretion of tumor necrosis factor alpha (TNF-alpha) and the neuroend

192 In the current study, we identified tumor necrosis factor alpha (TNF-alpha) as a major facto

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

194 f producing gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) but not interleu

195 hat responds to inflammatory stimuli such as tumor necrosis factor alpha (TNF-alpha) by initiating a

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

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

198 matoid arthritis show inadequate response to tumor necrosis factor alpha (TNF-alpha) inhibitors; litt

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

200 (CARHSP1), which regulates the stability of tumor necrosis factor alpha (TNF-alpha) mRNA.

201 Cells were treated either with sensitizing tumor necrosis factor alpha (TNF-alpha) or Stx2a, a sequ

202 f bronchoalveolar lavage fluid revealed that tumor necrosis factor alpha (TNF-alpha) release and cell

203 uman monocyte cell line, markedly suppressed tumor necrosis factor alpha (TNF-alpha) secretion in res

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

205 he 25 targets predicted by network analysis, tumor necrosis factor alpha (TNF-alpha) was firstly expe

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

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

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

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

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

211 nula occluden 1 (ZO-1), occludin, claudin-2, tumor necrosis factor alpha (TNF-alpha), and interleukin

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

213 IKKbeta) and IkappaBalpha in the presence of tumor necrosis factor alpha (TNF-alpha), confirming the

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

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

216 for the proinflammatory cytokines IL-1beta, tumor necrosis factor alpha (TNF-alpha), IL-10, and IL-6

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

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

219 the role of interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), two factors pro

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

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

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

223 We demonstrated previously that tumor necrosis factor alpha (TNF-alpha)-producing Chlamy

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

225 ed CD107a, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha).

226 ion was dependent on autocrine production of tumor necrosis factor alpha (TNF-alpha).

227 the induction of apoptosis by treatment with tumor necrosis factor alpha (TNF-alpha).

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

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

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

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

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

233 ere, we examined how the inflammatory factor tumor necrosis factor-alpha (TNF-alpha) broadly modulate

234 Furthermore, FKGK18 inhibited production of tumor necrosis factor-alpha (TNF-alpha) from CD4(+) T ce

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

236 Tumor necrosis factor-alpha (TNF-alpha) is a proalgesic

237 Tumor necrosis factor-alpha (TNF-alpha) is a proinflamma

238 ptor for advanced glycation end products and tumor necrosis factor-alpha (TNF-alpha) levels were also

239 h reduced NOX3 expression, STAT1 activation, tumor necrosis factor-alpha (TNF-alpha) levels, and apop

240 -77 exhibited increased abundance of adipose tumor necrosis factor-alpha (TNF-alpha) mRNA and impaire

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

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

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

244 The serum contains high levels of tumor necrosis factor-alpha (TNF-alpha) that selectively

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

246 vels of two cytokines (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)), one soluble cy

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

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

249 ring T-cell expression of CD107a, IFN-gamma, tumor necrosis factor-alpha (TNF-alpha), and IL-2.

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

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

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

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

254 arrying shRNA to AAT1, and then treated with tumor necrosis factor-alpha (TNF-alpha).

255 by proinflammatory cytokines, including the tumor necrosis factor-alpha (TNF-alpha).

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

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

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

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

260 nd levels of biomarkers (C-reactive protein, tumor necrosis factor alpha [TNF-alpha], interleukin 6 [

261 Production of proinflammatory cytokines (tumor necrosis factor alpha [TNF-alpha], interleukin-6 [

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

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

264 e immunoglobulin G Fc receptor II (FcGR) and tumor necrosis factor-alpha (TNFA) genes are known to in

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

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

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

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

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

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

271 Tumor necrosis factor alpha (TNFalpha) is a major proinf

272 ermal growth factor receptor (EGFR)/ErbB and tumor necrosis factor alpha (TNFalpha) receptor (TNFR) f

273 ectively inhibited LPS-induced hemolysis and tumor necrosis factor alpha (TNFalpha) secretion in a co

274 1/2) activation (i.e. phosphorylation) links tumor necrosis factor alpha (TNFalpha) to pro-inflammato

275 Furthermore, tumor necrosis factor alpha (TNFalpha) was elevated in d

276 Among these were tumor necrosis factor alpha (TNFalpha), CCL2, CXCL10, IL

277 regulation by the proinflammatory cytokines tumor necrosis factor alpha (TNFalpha), interleukin-1bet

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

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

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

281 sponsive to established treatments targeting tumor necrosis factor alpha (TNFalpha).

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

283 Tumor necrosis factor-alpha (TNFalpha) mediated IKKbeta

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

285 All brain regions showed increased levels of tumor necrosis factor-alpha (TNFalpha) protein by 45 hr,

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

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

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

289 tumor burden in mutant mice was dependent on tumor necrosis factor-alpha (TNFalpha), a tumorigenic, N

290 -and-puncture models of sepsis, but not in a tumor necrosis factor-alpha (TNFalpha)-induced sepsis mo

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

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

293 nflammation score; FR: interleukin-1beta and tumor necrosis factor alpha) vs. O-SED.

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

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

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

297 the inflammatory cytokines IL-1B, IL-6, and tumor necrosis factor-alpha were increased in panc-PTP1B

298 mmunoglobulin E, interleukin (IL)-1beta, and tumor necrosis factor-alpha were shown in the plant stan

299 roinflammatory cytokines IL-6, IL-1beta, and tumor necrosis factor-alpha, whereas coinfected DCs did

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