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

1 sed production of proinflammatory cytokines (tumor necrosis factor-alpha).

2 including interleukin (IL)-1beta, IL-6, and tumor necrosis factor alpha.

3 /MRI before and after ILP with melphalan and tumor necrosis factor-alpha.

4 to an increase of IL-1beta and a decrease of tumor necrosis factor-alpha.

5 chemokine (C-C motif) ligand 2 (CCL2)], and tumor necrosis factor-alpha.

6 enes more modestly for IL-17, and weakly for tumor necrosis factor-alpha.

7 its inflammation by gene expression of TNF (tumor necrosis factor)-alpha.

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

9 atment resulted in enhanced plasma levels of tumor necrosis factor-alpha (+53%; p = 0.02), interleuki

10 acetylsalicylic acid increased production of tumor necrosis factor-alpha (+66%) and decreased product

11 activated receptor agonists and inhibited by tumor necrosis factor alpha, a cytokine that causes insu

12 ymphopoietin, endothelin-1, and inflammatory tumor necrosis factor-alpha activated distinct but overl

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

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

15 Serum levels of tumor necrosis factor -alpha and interferon-gamma were s

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

17 expression of the proinflammatory cytokines tumor necrosis factor alpha and interleukin-1beta in lun

18 its metabolites suppressed the secretion of tumor necrosis factor alpha and interleukin-6 mediated t

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

20 t pathway activation and decreased levels of tumor necrosis factor alpha and monocyte chemoattractant

21 s those observed in ECD kidneys, except that tumor necrosis factor alpha and monocyte chemotactic pro

22 hage inflammatory protein-1alpha and -1beta; tumor necrosis factor-alpha and -R2), endothelial injury

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

24 nf or Ccl3 expression in marrow and elevated tumor necrosis factor-alpha and chemokine (C-C motif) li

25 D-loop content was directly proportional to tumor necrosis factor-alpha and high-mobility group prot

26 -active form of antibodies to S-100 protein, tumor necrosis factor-alpha and histamine, (Kolofort) un

27 ammatory cytokines (including interleukin-6, tumor necrosis factor-alpha and interleukin-1beta), reba

28 onin levels and decreased nuclear factor-kB, tumor necrosis factor-alpha and interleukin-6 gene expre

29 including corticosteroids and inhibitors of tumor necrosis factor-alpha and interleukin-6.

30 Inflammatory mediators, like tumor necrosis factor-alpha and prostaglandin E(2) , inc

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

32 Moreover, the expressions of TNF-alpha (tumor necrosis factor-alpha) and IFN-gamma (interferon-g

33 tive protein, interleukin 6, interleukin 10, tumor necrosis factor alpha), and the measures were aver

34 CXCL8 (IL-8), IL-6, TNF-alpha (tumor necrosis factor-alpha), and IL-10 release was meas

35 ivator of transcription proteins), TNFalpha (tumor necrosis factor-alpha), and T-cell receptor signal

36 -inflammatory cytokines, including IL-1beta, tumor necrosis factor alpha, and IL-6, and this inductio

37 helin-1 along with interleukin (IL)-6, IL-8, tumor necrosis factor alpha, and interferon gamma-induce

38 locyte macrophage-colony-stimulating factor, tumor necrosis factor alpha, and interleukin (IL)-6 secr

39 ncluding monocyte chemoattractant protein 1, tumor necrosis factor alpha, and interleukin 6) through

40 ction of monocyte chemoattractant protein-1, tumor necrosis factor alpha, and interleukin-6 from mous

41 s concomitant with an impaired production of tumor necrosis factor alpha, and interleukins 6 and 12 (

42 ases in interleukin 1beta, interferon gamma, tumor necrosis factor alpha, and ionized calcium binding

43 soluble CD25, interleukin (IL)-6, IL-1beta, tumor necrosis factor-alpha, and IL-10 and lower levels

44 e associated cytokines interleukin-6 (IL-6), tumor necrosis factor-alpha, and IL-1beta also showed an

45 Interleukin-6 and -10, tumor necrosis factor-alpha, and insulin-like growth fac

46 ation, and interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and interleukin-10 levels i

47 inflammatory biomarkers-C-reactive protein, tumor necrosis factor-alpha, and interleukins-6, -8, and

48 flammatory factors, including interleukin-6, tumor necrosis factor-alpha, and matrix metalloproteinas

49 n human or mouse keratinocytes by IL-1alpha, tumor necrosis factor-alpha, and phorbol myristate aceta

50 cytokines interleukin-1beta, interleukin-12, tumor necrosis factor-alpha, and reactive oxygen species

51 mice had higher levels of interleukin-1beta, tumor necrosis factor-alpha, and reactive oxygen species

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

53 effectiveness of vedolizumab (VDZ) and anti-tumor necrosis factor alpha (anti-TNFalpha) in UC and CD

54 (IL [interleukin]-1beta, IL-6, and TNFalpha [tumor necrosis factor alpha]), as well as NF-kappaB (nuc

55 Tumor necrosis factor alpha but not IL-1beta had a profo

56 macrophage inflammatory protein 1 alpha, and tumor necrosis factor alpha, but not IL-6.

57 mpens secretion of the inflammatory cytokine tumor necrosis factor-alpha by microglial cells in the f

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

59 Interleukin-6, -8, and -10, tumor necrosis factor-alpha, C-reactive protein, and S-1

60 -6, -8, and -10 retained the association but tumor necrosis factor-alpha, C-reactive protein, and S-1

61 ervention group, interleukin-6, -8, and -10, tumor necrosis factor-alpha, C-reactive protein, and S-1

62 erferon (IFN)-gamma, interleukin (IL)1-beta, tumor necrosis factor alpha, caspase-1 (CASP1), intercel

63 ed with decreased early gut injury and serum tumor necrosis factor-alpha compared with allogeneic con

64 ylsalicylic acid prophylaxis enhanced plasma tumor necrosis factor-alpha concentrations upon the firs

65 chia, and showed increased interleukin-8 and tumor necrosis factor-alpha concentrations.

66 The metalloprotease TACE (tumor necrosis factor alpha converting enzyme) is respon

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

68 ogical suppression of the Nrg1TIII inhibitor tumor necrosis factor-alpha-converting enzyme (TACE/ADAM

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

70 sceral fat and the pro-inflammatory cytokine tumor necrosis factor alpha correlated with spatial memo

71 Tumor necrosis factor-alpha coupled with NGR (NGR-hTNF),

72 ors, including interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha, cyclooxygenase-2, and phosp

73 sponse characterized by interferon-gamma and tumor necrosis factor-alpha cytokine secretion by CD4(+)

74 itor of the proinflammatory cytokine soluble tumor necrosis factor alpha days after an injury suffici

75 Furthermore, tumor necrosis factor-alpha decreased both mineralocorti

76 pstream of LITAF (lipopolysaccharide-induced tumor necrosis factor-alpha factor), a protein encoding

77 r protein in neurons and in the secretion of tumor necrosis factor-alpha from microglial cells.

78 Moreover, rs1799964 SNP at tumor necrosis factor-alpha gene in CZS babies is associ

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

80 gulation of the extrinsic apoptotic pathway- tumor necrosis factor alpha -> nuclear factor kappaB ->

81 This study compares levels of tumor necrosis factor alpha, IL-6, and IL-8 in criticall

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

83 Proinflammatory cytokines tumor necrosis factor-alpha, IL-1beta, IL-6, and IL-12p4

84 sed inflammatory genes (NF-kappaB, TNFalpha [tumor necrosis factor alpha], IL-1alpha) and in vivo lip

85 Here we investigate a new role for tumor necrosis factor alpha in promoting N-glycan-proces

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

87 levels of p21, mTOR/pS6, interleukin 6, and tumor necrosis factor alpha in skin and heart tissues of

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

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

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

91 Both compounds also reduced the tumor necrosis factor alpha-induced activation of NF-kap

92 O hepatocytes were sensitized to ethanol and tumor necrosis factor alpha-induced mitochondrial dysfun

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

94 A20 (tumor necrosis factor alpha-induced protein 3 or TNFAIP3

95 TIPE2 (tumor necrosis factor alpha-induced-protein 8-like 2), i

96 nnel fluorescence intravital microscopy of a tumor necrosis factor-alpha-induced acute inflammation m

97 tor T cell-mediated and interferon-gamma and tumor necrosis factor-alpha-induced cell death compared

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

99 We now show that tumor necrosis factor-alpha-induced Txnip degradation in

100 Furthermore, the tumor-necrosis-factor-alpha-inducing activity of the lip

101 Tumor necrosis factor alpha inhibitors (TNFi) are common

102 with disseminated histoplasmosis were taking tumor necrosis factor alpha inhibitors.

103 articularly among patients who are receiving tumor necrosis factor alpha inhibitors.

104 an immunodeficiency virus, on dialysis, with tumor necrosis factor-alpha inhibitors, who had an organ

105 vel, metformin lowered ex vivo production of tumor necrosis factor alpha, interferon gamma, and inter

106 ncentrations (interleukin [IL]-21, IL-1beta, tumor necrosis factor-alpha, interferon-gamma) and CCR5,

107 induced proinflammatory cytokines, including tumor necrosis factor alpha, interleukin 1beta (IL-1beta

108 roduction of the cytokines interferon gamma, tumor necrosis factor alpha, interleukin 4, and interleu

109 ession of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin-10 (IL-10), IL-

110 alpha1), and fibronectin while up-regulating tumor necrosis factor alpha, interleukin-6, and C-X-C mo

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

112 BCG-disA-OE elicited significantly stronger tumor necrosis factor-alpha, interleukin (IL)-6, IL-1bet

113 ystems, inflammatory cytokines on perfusate (tumor necrosis factor-alpha, interleukin [IL]-1B, IL-6,

114 rogenase, total bilirubin) and inflammation (tumor necrosis factor-alpha, interleukin-10).

115 ins such as inducible nitric oxide synthase, tumor necrosis factor-alpha, interleukin-1beta, and inte

116 of multiple inflammatory markers, including tumor necrosis factor-alpha, interleukin-1beta, and nitr

117 easurement of systemic inflammatory markers (tumor necrosis factor-alpha, interleukin-6).

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

119 ated inflammatory gene expression (IL-1beta, tumor necrosis factor-alpha, intracellular adhesion mole

120 loop between TAMs and cancer cells driven by tumor necrosis factor alpha involving SIGLEC1 and CCL8,

121 ation and injury in the cerebrospinal fluid (tumor necrosis factor-alpha, kynurenic acid, tau).

122 bation of these BDOs with interleukin 17A or tumor necrosis factor alpha led to an immune-reactive ph

123 CB(2) -R activation also decreased serum tumor necrosis factor-alpha levels and improved cardiac

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

125 % confidence interval {CI}, .37-.78]), IL-16/tumor necrosis factor-alpha (OR, 0.66 [95% CI, .45-.93])

126 ury and could not produce interleukin-1beta, tumor necrosis factor-alpha, or reactive oxygen species.

127 2 was related to biomarkers of inflammation (tumor necrosis factor alpha [P = .007]), monocyte/macrop

128 eased vessel density in the penumbra, higher tumor necrosis factor alpha plasma levels and lower peri

129 interferon gamma-positive [IFN-gamma(+)] and tumor necrosis factor alpha-positive [TNF-alpha(+)]), an

130 Tumor necrosis factor-alpha potentiated thymic stromal l

131 The frequency of tumor necrosis factor alpha-producing, interleukin 6 (IL

132 1 and induced Toll-like receptor 4-dependent tumor necrosis factor alpha production by macrophages.

133 tokine and chemokine expression and prolongs tumor necrosis factor alpha production on the inflammato

134 FN generation differentially correlated with tumor necrosis factor alpha production.

135 cells demonstrated impaired interferon-gamma/tumor necrosis factor-alpha production at relapse, which

136 ne-exposed cells showed increased TNF-alpha (tumor necrosis factor-alpha) production.

137 We show that tumor necrosis factor alpha receptor 1 (TNFR1) in the pa

138 Of the six biomarkers examined, only tumor necrosis factor alpha receptor 1 showed a signific

139 azard ratio, 1.26 [95% CI, 1.13-1.42]), TNF (tumor necrosis factor)-alpha receptor 1 (hazard ratio, 1

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

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

142 , and interleukin 2-, interferon gamma-, and tumor necrosis factor alpha-secreting T-cell responses w

143 splenocytes show higher interferon-gamma and tumor necrosis factor-alpha secretion upon antigen re-st

144 Here we show subsets of the IL-17 and tumor necrosis factor-alpha signaling pathways are robus

145 r cytokine (interleukin-2, interferon-gamma, tumor necrosis factor-alpha) staining assays after in vi

146 molecule)-1 and TF expression following TNF (tumor necrosis factor)-alpha stimulation.

147 The cytokine soluble tumor necrosis factor alpha (sTNFalpha) is upregulated i

148 steoprotegerin]), 3 inflammatory biomarkers (tumor necrosis factor-alpha, sTNFRI [soluble tumor necro

149 ced glycation end products, interleukin-1ra, tumor necrosis factor alpha, surfactant protein D, and i

150 is a human monoclonal antibody specific for tumor necrosis factor alpha that has already been approv

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

152 Previously, we reported that tumor necrosis factor-alpha time-dependently alters CLDN

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

154 Here, we find that tumor necrosis factor alpha (TNF-alpha) acts differently

155 gut in response to injury provoked by murine tumor necrosis factor alpha (TNF-alpha) and 5-Fluorourac

156 pression in hypothalamic microglia including tumor necrosis factor alpha (TNF-alpha) and interleukin

157 ted lipopolysaccharide-induced expression of tumor necrosis factor alpha (TNF-alpha) and interleukin-

158 tivity and also with decreased production of tumor necrosis factor alpha (TNF-alpha) and interleukin-

159 occi was associated with decreased levels of tumor necrosis factor alpha (TNF-alpha) and lowered expr

160 VEC was similar under control conditions but tumor necrosis factor alpha (TNF-alpha) and PKCdelta-i h

161 Potent agonists of NF-kappaB such as tumor necrosis factor alpha (TNF-alpha) and vgRNA failed

162 We identified tumor necrosis factor alpha (TNF-alpha) as the key aging

163 adhesion to endothelial cells inflamed with tumor necrosis factor alpha (TNF-alpha) by reducing expr

164 of CD107a, gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) from ILC3; and a

165 Specifically, inhibitors to tumor necrosis factor alpha (TNF-alpha) include etanerce

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

167 ulation of interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) mRNA and increas

168 containing 223Q significantly decreased both tumor necrosis factor alpha (TNF-alpha) mRNA levels and

169 ion levels of proinflammatory cytokines like tumor necrosis factor alpha (TNF-alpha) or interleukin-6

170 Genetic knockout of tumor necrosis factor alpha (TNF-alpha) or pharmacologic

171 lical vein ECs, we found that treatment with tumor necrosis factor alpha (TNF-alpha) or the strong ox

172 s decreased interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production.

173 classes were shown to promote TLR2-dependent tumor necrosis factor alpha (TNF-alpha) release from bon

174 transactivate a NF-kappaB reporter following tumor necrosis factor alpha (TNF-alpha) stimulation, con

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

176 ive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were also evalua

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

178 Here, we show that tumor necrosis factor alpha (TNF-alpha), a critical cyto

179 n designed, developed, and characterized for tumor necrosis factor alpha (TNF-alpha), a protein bioma

180 e induction, including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and CXCL8, and

181 y, we measured interleukin (IL) 1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and high-sensit

182 yte colony-stimulating factor (GCSF), MCP-1, tumor necrosis factor alpha (TNF-alpha), and IgG anti-to

183 in E. faecalis-induced DCs, while IL-1beta, tumor necrosis factor alpha (TNF-alpha), and IL-12 level

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

185 f secretion of gamma interferon (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin

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

187 h levels of gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), as well as a ra

188 several cytokines and chemokines, especially tumor necrosis factor alpha (TNF-alpha), CCL3, CCL4, and

189 ly, interleukin 1beta (IL-1beta), IL-10, and tumor necrosis factor alpha (TNF-alpha), consistent with

190 ukin 1alpha (IL-1alpha), IL-6, IL-9, RANTES, tumor necrosis factor alpha (TNF-alpha), CXCL1, CXCL2, C

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

192 and CD8(+) T cells producing high levels of tumor necrosis factor alpha (TNF-alpha), gamma interfero

193 1-RIPK3-MLKL signaling cascade downstream of tumor necrosis factor alpha (TNF-alpha), has been implic

194 get classes, including interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-alpha), IL-6, IL-12/23,

195 ytokine profile dominated by cytokines IL-2, tumor necrosis factor alpha (TNF-alpha), or IL-17 but la

196 e PA total effect was mediated through IL-6, tumor necrosis factor alpha (TNF-alpha), or TNF-alpha re

197 ation of seminiferous tubules, and increased tumor necrosis factor alpha (TNF-alpha), particularly in

198 in old mice and increased systemic levels of tumor necrosis factor alpha (TNF-alpha), which functions

199 ype 1-matrix metalloproteinase (MT1-MMP) and tumor necrosis factor alpha (TNF-alpha)-converting enzym

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

201 genes and potentiates toxicity triggered by tumor necrosis factor alpha (TNF-alpha).

202 ukin 10 (IL-10), interleukin 22 (IL-22), and tumor necrosis factor alpha (TNF-alpha).

203 that express interleukin-2 (IL-2), IL-4, and tumor necrosis factor alpha (TNF-alpha).

204 RelA could be reversed by neutralization of tumor necrosis factor alpha (TNF-alpha).

205 phages in response to lipopolysaccharide and tumor necrosis factor alpha (TNF-alpha).

206 cluding interleukin 6 (IL-6), IL-1alpha, and tumor necrosis factor alpha (TNF-alpha).

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

208 ene expression changes induced by short-term tumor necrosis factor-alpha (TNF) treatment were largely

209 nflammatory cytokines (interleukin-6 (IL-6); tumor necrosis factor-alpha (TNF)).

210 ation with proinflammatory cytokines such as tumor necrosis factor-alpha (TNF), the master transcript

211 m samples were used to measure the levels of tumor necrosis factor-alpha (TNF-alpha) and cytokine-ind

212 sponsible for the cleavage of membrane-bound tumor necrosis factor-alpha (TNF-alpha) and its receptor

213 ian carcinoma tissues express high levels of tumor necrosis factor-alpha (TNF-alpha) and other inflam

214 that sheds both the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and TNF receptor

215 viously demonstrated that supraphysiological tumor necrosis factor-alpha (TNF-alpha) boosts glutamate

216 d production of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) by microglia whe

217 ) have been found to have elevated levels of Tumor Necrosis Factor-alpha (TNF-alpha) in the eye.

218 1 beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the gingival

219 ophage-colony stimulating factor (M-CSF) and tumor necrosis factor-alpha (TNF-alpha) in vitro by isol

220 levels but positively correlated with plasma tumor necrosis factor-alpha (TNF-alpha) levels at 8 to 1

221 ascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-alpha) may regulate sev

222 n pro-inflammatory gene expression following tumor necrosis factor-alpha (TNF-alpha) or interkeukin-1

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

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

225 tem can be used to profile downregulation of tumor necrosis factor-alpha (TNF-alpha) secretion by sin

226 In adults, anti-tumor necrosis factor-alpha (TNF-alpha) therapy is assoc

227 -fold (CI, 1.3- to 40.0-fold; P < 0.001) for tumor necrosis factor-alpha (TNF-alpha), 7.0-fold (CI, 3

228 flammatory biomarkers [interleukin-6 (IL-6), Tumor Necrosis Factor-Alpha (TNF-alpha), and C-reactive

229 cretion from GF was evaluated in response to tumor necrosis factor-alpha (TNF-alpha), IL-1beta, Esche

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

231 inflammatory markers (interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 r

232 serum GSH and inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1be

233 dition, C-L reduces the expression levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (

234 he transcription factor T-bet in response to tumor necrosis factor-alpha (TNF-alpha), which was rapid

235 SLURP1 blocked the tumor necrosis factor-alpha (TNF-alpha)-activated dHL-60

236 -coated particles decreased the secretion of tumor necrosis factor-alpha (TNF-alpha).

237 l growth factor (VEGF) and can be induced by tumor necrosis factor-alpha (TNF-alpha).

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

239 nflammatory interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha).

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

241 ines (e.g., interferon gamma [IFN-gamma] and tumor necrosis factor alpha [TNF-alpha]) produced by inn

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

243 inflammatory markers (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-alpha], interleukin-1 r

244 er infection resulted in an earlier onset of tumor necrosis factor-alpha (TNFa)-mediated bladder infl

245 on plasma concentrations of proinflammatory tumor necrosis factor alpha (TNFalpha) and interferon-ga

246 ate activation of proinflammatory cytokines (tumor necrosis factor alpha (TNFalpha) and interleukin 6

247 vate THP-1 human monocytic cells to generate tumor necrosis factor alpha (TNFalpha) and interleukin 8

248 ect against lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFalpha) and interleukin-1

249 xamined 5' UTR transcriptional regulation by tumor necrosis factor alpha (TNFalpha) and interleukin-1

250 rum infected erythrocytes (IE) interact with tumor necrosis factor alpha (TNFalpha) and thrombin in t

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

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

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

254 Tumor necrosis factor alpha (TNFalpha) has emerged as a

255 e expression of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) in gut-associated

256 Although ER stress-inducing drugs or tumor necrosis factor alpha (TNFalpha) in rat chondrosar

257 Microinjection of tumor necrosis factor alpha (TNFalpha) in the brain pare

258 2) Tumor necrosis factor alpha (TNFalpha) induced HA-mediat

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

260 Tumor necrosis factor alpha (TNFalpha) is a soluble cyto

261 Tumor necrosis factor alpha (TNFalpha) is important for

262 s a previously unrecognized component of the tumor necrosis factor alpha (TNFalpha) receptor 1 signal

263 kines in response to interleukin-1 (IL-1) or tumor necrosis factor alpha (TNFalpha) stimulation.

264 1/2) activation (i.e. phosphorylation) links tumor necrosis factor alpha (TNFalpha) to pro-inflammato

265 DR), but not NF-kappaB activation induced by tumor necrosis factor alpha (TNFalpha), interleukin (IL)

266 nd metalloprotease 17) is a key regulator of tumor necrosis factor alpha (TNFalpha), interleukin 6 re

267 of acute brain inflammation induced by local tumor necrosis factor alpha (TNFalpha), we found that up

268 ase (iNOS), Interleukin 1beta (IL-1beta) and Tumor Necrosis Factor Alpha (TNFalpha), were assessed.

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

270 st normal and tumor cells are protected from tumor necrosis factor alpha (TNFalpha)-induced apoptosis

271 In this issue of Blood, He et al show that a tumor necrosis factor alpha (TNFalpha)-mediated pathway

272 ines as potent, small molecule inhibitors of tumor necrosis factor alpha (TNFalpha).

273 es the skeleton to the osteolytic effects of tumor necrosis factor alpha (TNFalpha).

274 0 g pellet contained a significant amount of tumor necrosis factor alpha (TNFalpha).

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

276 o immunomodulators (ie, thiopurines) or anti-tumor necrosis factor-alpha (TNFalpha) therapy.

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

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

279 e H3 (AC-H3), histone deacetylase 1 (HDAC)1, tumor necrosis factor-alpha (TNFalpha), and Toll-like re

280 Tumor necrosis factor-alpha (TNFalpha), known to be incr

281 ted modest p38 activation, but did not alter tumor necrosis factor-alpha (TNFalpha)-induced p38 activ

282 etween DNA and the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFalpha).

283 duction of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha).

284 nflammatory molecules (interleukin-6 [IL-6], tumor necrosis factor alpha [TNFalpha], matrix metallopr

285 IL-17B cooperated with tumor necrosis factor-alpha to induce expression of neut

286 By applying exogenous tumor necrosis factor-alpha to mimic inflammation in vit

287 response to proinflammatory stimuli, such as tumor necrosis factor-alpha, Toll-like receptor ligands,

288 igh expression of lipopolysaccharide-induced tumor necrosis factor-alpha transcription factor 3 (LL3)

289 nase-2 were significantly increased, whereas tumor necrosis factor-alpha, transforming growth factor-

290 out EPC-derived exosome as well as TNFalpha (tumor necrosis factor-alpha)-treated mouse cardiac endot

291 muscle actin expression induced by prolonged tumor necrosis factor-alpha treatment, because they were

292 y release of cytokines (interferon-gamma and tumor necrosis factor-alpha), upregulation of surface CD

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

294 h an antibody, the target cytokine, that is, tumor necrosis factor-alpha, was measured in terms of ro

295 y markers (interleukin [IL]-1beta, IL-6, and tumor necrosis factor-alpha) were observed in the medium

296 markers: inducible nitric-oxide synthase and tumor necrosis factor-alpha, when cultured under hypergl

297 serum levels of IL-23, IFN-beta, MCP-1, and tumor necrosis factor-alpha, whereas 1866 reduced IFN-ga

298 ry response mediators (interleukin-1beta and tumor necrosis factor alpha), which are associated with

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

300 nsing platform through the quantification of tumor necrosis factor alpha with a detection limit as lo