ライフサイエンスコーパス: TNF-alpha

1 TNF-alpha (but not IL5, IL-3, eotaxin-1 or GM-CSF) was d

2 TNF-alpha is a pluripotent cytokine that has been indepe

3 TNF-alpha related apoptosis-inducing ligand (TRAIL) sele

4 TNF-alpha treatment of colonic rho(0) cells augmented IL

5 TNF-alpha was injected intraperitoneally, with or withou

6 TNF-alpha was not detected in Muller cells from diabetic

7 monocyte chemoattractant protein 1 (MCP-1), TNF-alpha, and IL-6 and hepatic cleaved caspase 3 in mic

8 IL-1, TNF-alpha, and estrogen stimulate release of Hsp90 and a

9 s tested but urokinase was released by IL-1, TNF-alpha, and thrombin (positive control), but not estr

10 6, FOXP3), cytokines (IL-1beta, IL-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismutase, c

11 ma, IL-2, IL-6, and IL-1beta) or low (IL-15, TNF-alpha, IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10,

12 up-regulated cytokines, including IL-1beta, TNF-alpha and IL-6 in various CNS regions.

13 pression of pro-inflammatory genes IL-1beta, TNF-alpha and iNOS.

14 jun and p38 activation, as well as IL-1beta, TNF-alpha, and IL-10 secretion in vascular endothelial c

15 induced a significant increase in IL-1beta, TNF-alpha, and IL-6 messenger RNA (mRNA) expression and

16 Salivary concentrations of IL-1beta, TNF-alpha, and MMP-2/TIMP-2 complex were assessed using

17 M. tuberculosis-specific IFN-gamma(+)IL-2(-)TNF-alpha(+) CD4 T cells.

18 ted with reduced inflammation (MCP-1, MIP-2, TNF-alpha, IL-6 and CD68), decreased accumulation of bon

19 ammatory cytokines (e.g. IL-6, MCP-1, IL-22, TNF-alpha) and pronounced complement consumption, resemb

20 inly) and eosinophils and secretion of IL-6, TNF-alpha, and IL-17 in contrast to the eosinophilic inf

21 of IL-32 expression with expression of IL-6, TNF-alpha, IL-8, and cyclooxygenase-2 was also investiga

22 , MCL down-regulated the expression of IL-6, TNF-alpha, MCP-1/CCL2 and IFN-gamma in sera, and amelior

23 orn to obese mothers generate a reduced IL-6/TNF-alpha response to TLR 1/2 and 4 ligands compared to

24 CH suppressed IL-1beta, IL-6, IL-8, TNF-alpha and COX-2, while PPH reduced LPS-induced IL-6

25 (66.4%) and/or tumor necrosis factor alpha (TNF-alpha) (63.7%).

26 cells secreting tumor necrosis factor alpha (TNF-alpha) but not interferon gamma or interleukin 2 whi

27 spine size are tumor necrosis factor alpha (TNF-alpha) dependent and thus are likely associated with

28 ide (AICAR), on tumor necrosis factor alpha (TNF-alpha) induction of complement factor B (CFB) in RPE

29 (IFN)-gamma and tumor necrosis factor alpha (TNF-alpha) that induced tumor cell growth arrest.

30 (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) were delayed and low in CAST mice compared to

31 he detection of tumor necrosis factor alpha (TNF-alpha) within the randomly chosen range of 266pg/mL

32 XCL2, IL-1beta, tumor necrosis factor alpha (TNF-alpha), and IL-6.

33 on (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin 2 (IL-2) secretion by CD8(+)

34 ma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin-2 (IL-2) (P < 0.001) and spl

35 kin (IL) 1beta, tumor necrosis factor alpha (TNF-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase

36 d SseK3 inhibit tumor necrosis factor alpha (TNF-alpha)-induced NF-kappaB activation.

37 treatment with tumor necrosis factor alpha (TNF-alpha)-neutralizing antibodies decreased the frequen

38 lls primed with tumor necrosis factor alpha (TNF-alpha).

39 e production of tumor necrosis factor alpha (TNF-alpha)/interleukin-6 (IL-6) in infected kidneys.

40 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha) play key roles in progression of renal fibros

41 wnregulation of tumor necrosis factor-alpha (TNF-alpha) production and concomitant upregulation of NF

42 igher level of tumour-necrosis factor-alpha (TNF-alpha) secretion and markedly reduced neuronal viabi

43 Tumor necrosis factor-alpha (TNF-alpha) stimulation can increase miR-19a expression,

44 ion of ECs with tumor-necrosis factor-alpha (TNF-alpha) the supernatants of EC cultures were subjecte

45 in-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)), were analyzed in maternal and umbilical cor

46 L-1beta), IL-6, tumor necrosis factor-alpha (TNF-alpha), and chemokine (C-X-C motif) ligand 8 (CXCL8)

47 eukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and vascular endothelial growth factor peake

48 gulated retinal tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta), intracellular

49 and release of tumor necrosis factor-alpha (TNF-alpha).

50 on [IFN-gamma], tumor necrosis factor alpha [TNF-alpha], and interleukin-2 [IL-2]) and type 17 (IL-17

51 ression of A20 (tumor necrosis factor alpha [TNF-alpha]-induced protein 3 [TNFAIP3]), an inhibitor of

52 eta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and IL-6) by quantitative reverse transcript

53 egulated TLR2 (P <0.05), RAGE (P <0.01), and TNF-alpha (P <0.05) relative to the sites with experimen

54 IL-1 and TNF-alpha stimulate release of urokinase, which can conv

55 ile CD1(-) cDC secreted IFN-alpha, IL-12 and TNF-alpha.

56 3 induces the production of IL-6, IL-13, and TNF-alpha.

57 markers synergistically induced by IL-17 and TNF-alpha (IL-17A/C, IL-19, CXCL1, PI3, CCL20, and IL36G

58 y cytokines including IL-4, IL-13, IL-17 and TNF-alpha.

59 clear phagocytes with increased IL-1beta and TNF-alpha content, (3) a TH17 bias of CD4(+) T cells, (4

60 educed NF-kappaB translocation, IL-1beta and TNF-alpha expression, and production (p < 0.001).

61 ar translocation and downstream IL-1beta and TNF-alpha protein production following TLR2 receptor sti

62 on of the proinflammatory proteins COX-2 and TNF-alpha.

63 gmented IFN-gamma, interleukin-2 (IL-2), and TNF-alpha production.

64 nd IL-21, and to a lesser extent by IL-4 and TNF-alpha.

65 nterfering RNA enhanced LPS-induced IL-6 and TNF-alpha expression.

66 MYD2 might be induced by cyst fluid IL-6 and TNF-alpha in ADPKD kidneys.

67 ibrinogen, the expression levels of IL-6 and TNF-alpha in integrin alphaM(PS)beta2 BMDMs were signifi

68 ation of IL-10 increased IFN-gamma, IL-6 and TNF-alpha production and improved bacteria killing.

69 OX-2, while PPH reduced LPS-induced IL-6 and TNF-alpha responses.

70 Both IL-6 and TNF-alpha were lower at 1 h than at 4 h of the peritonea

71 iency though plasma levels of IL-4, IL-6 and TNF-alpha were slightly affected by 11beta-HSD1 deficien

72 a, reduced epithelial expression of IL-6 and TNF-alpha, and impaired bacterial clearance.

73 uctions of IL-17 and IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels were increased in periph

74 brain and microglial production of IL-6 and TNF-alpha.

75 ipheral blood monocyte secretion of IL-6 and TNF-alpha.

76 Serum and GCF endocan, VEGF-A, and TNF-alpha levels were significantly higher in patients w

77 tion between GCF endocan levels, VEGF-A, and TNF-alpha levels with periodontal probing depth (PD).

78 However, T. gondii inhibited IFN-alpha and TNF-alpha produced in response to HSV and HIV, thus func

79 vity also failed to up-regulate IFN-beta and TNF-alpha after treatment with DMXAA or the natural STIN

80 c fibroblasts (MEFs) suppressed IFN-beta and TNF-alpha induction following stimulation with the STING

81 nal fibrosis, dual blockade of TGF-beta1 and TNF-alpha is desired as its therapeutic approach.

82 ect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokines while restoring MCP-2 levels, sugges

83 Additionally, BPA and TNF-alpha levels in cord blood were inversely associated

84 n this article, we demonstrate that CCL2 and TNF-alpha, inflammatory mediators that are elevated in t

85 mote areas together with clusterin (CLU) and TNF-alpha.

86 thways activated in human inflamed colon and TNF-alpha-treated cells (false discovery rate < 0.05).

87 igger Ab-dependent NK cell degranulation and TNF-alpha but not cytotoxicity or IFN-gamma production,

88 Endocan and TNF-alpha levels, both in GCF and serum, increased from

89 IFN-gamma and TNF-alpha also affected expression of several microRNAs

90 vo atherosclerotic tissue with IFN-gamma and TNF-alpha and found they synergistically increased monoc

91 uction in human blood, whereas IFN-gamma and TNF-alpha induction is largely TLR8-dependent.

92 to the inflammatory cytokines IFN-gamma and TNF-alpha led to inhibition of HNF-1beta transcriptional

93 lymphocytes, we observed less IFN-gamma and TNF-alpha production and T lymphocyte proliferation than

94 is occurred we observed higher IFN-gamma and TNF-alpha production than in nonblocked conditions.

95 early correlated inhibition of IFN-gamma and TNF-alpha production, along IL-10 increase, (ii) CD73(+)

96 that naive CAST mice make low IFN-gamma and TNF-alpha responses and have low levels of NK cells and

97 the pro-inflammatory cytokines IFN-gamma and TNF-alpha synergistically up-regulated PD-L1 expression.

98 y up-regulated miRNA following IFN-gamma and TNF-alpha treatment in HDLECs was miR-155, which has a c

99 on decreased the production of IFN-gamma and TNF-alpha, T cell proliferation, and the expression of C

100 cells upon activation through IFN-gamma and TNF-alpha.

101 IL-4, IFN-gamma, and TNF-alpha enhanced mucosal permeability in mice.

102 The effect of IL-4, IL-13, IFN-gamma, and TNF-alpha on mucosal permeability was tested in vivo.

103 GCF hs-CRP, IL-lbeta, and TNF-alpha levels were analyzed using an enzyme-linked im

104 nt particle sizes with dyes/QDs for LCN1 and TNF-alpha, we successfully used REP to detect the two DR

105 ation of p65, and suppressed basal level and TNF-alpha-induced expression of chemokines and adhesion

106 the lack of functional receptors for LPS and TNF-alpha.

107 results highlight CX3CR1(high) monocytes and TNF-alpha as potential therapeutic targets for preventin

108 ading to activation of the MyD88 pathway and TNF-alpha production.

109 ance, and decreased antigen presentation and TNF-alpha signaling, which may enable immune system avoi

110 T signalling system (5-HT, 5-HIAA, SERT) and TNF-alpha expression were examined in the distal colon o

111 ate nuclear factor (NF)-kappaB signaling and TNF-alpha production by targeting TNF alpha-induced prot

112 ond linkage of polymer P3 to immobilize anti-TNF alpha antibodies.

113 Anti-TNF-alpha/FNAB/PC membrane was integrated over array of

114 Anti-TNF-alpha/FNAB/PMMA matrix was then integrated over comb

115 ble to mount an immune response against anti-TNF-alpha Abs, suggesting that immune complexes are a ma

116 alent binding of capturing biomolecule (anti-TNF-alpha antibody) on off-surface matrix was achieved v

117 Last, in human and mouse colon, anti-TNF-alpha treatment restored reduced mitochondria-depend

118 ement in endothelial function following anti-TNF-alpha treatment (SDM 0.987, 95%CI [0.64-1.33], p < 0

119 , which are prevented by a neutralizing anti-TNF-alpha antibody.

120 er, neither TNF-alpha gene deletion nor anti-TNF-alpha neutralizing antibodies had any impact sustain

121 in the emergence of ADAs in the case of anti-TNF-alpha Abs.

122 meta-analysis to evaluate the effect of anti-TNF-alpha agents on endothelial function in RA patients.

123 Injection of anti-TNF-alpha neutralizing antibodies suppressed behavioral

124 ere we screened small molecules showing anti-TNF-alpha activity in the compound library of indole der

125 Recent studies have reported that anti-TNF-alpha therapy or RA itself can modulate AD pathology

126 tudies, our meta-analysis suggests that anti-TNF-alpha treatment may improve endothelial function in

127 The anti-TNF-alpha activity was mediated by inhibiting IkappaB ki

128 idrug Abs (ADA), directed against these anti-TNF-alpha Abs after just a few weeks of treatment.

129 -linker and further covalently binds to anti-TNF-alpha antibody via thermal reaction.

130 er (TNF-alpha) in undiluted serum using Anti-TNF-alpha/FNAB/PMMA/Au reveal that system can detect TNF

131 Compared with anti-TNF-alpha and cyclosporine, anti-IL-12/23 treatment resu

132 ns in the treatment of RA patients with anti-TNF-alpha drugs and in the potential use of TNF-targeted

133 ncluding RA patients; 3) treatment with anti-TNF-alpha medications; 4) evaluating the change from bas

134 thelial integrity, while treatment with anti-TNF-alpha or anti-IL-4Ralpha monoclonal antibodies resto

135 provide evidence that MenA inhibitors act as TNF-alpha and IL-6 inhibitors, raising the potential for

136 levels of proinflammatory cytokines, such as TNF-alpha and IL-17.

137 cation of proinflammatory cytokines, such as TNF-alpha, IL-1beta, IL-6, and IL-23.

138 roliferation, whereas Th1 cytokines, such as TNF-alpha, inhibit local ATM proliferation.

139 VEGF and pro-inflammatory cytokines such as TNF-alpha.

140 tegrity, while knockdown of USP48 attenuates TNF-alpha/JNK pathway and increases E-cadherin expressio

141 Results for estimating protein biomarker (TNF-alpha) in undiluted serum using Anti-TNF-alpha/FNAB/

142 ally, inhibition of dynamin activity blocked TNF-alpha-mediated infection.

143 nduced killing while simultaneously blocking TNF-alpha growth-promoting activities.

144 and activity are known to reduce both brain TNF-alpha [8] and offspring innate fear [9], whereas mat

145 l stress has been reported to increase brain TNF-alpha [10] and offspring fear and anxiety [11, 12],

146 ng fear and anxiety [11, 12], maternal brain TNF-alpha may report environmental conditions to promote

147 onally to its local actions in the AD brain, TNF-alpha can also indirectly modulate amyloid pathology

148 late homeostatic synaptic scaling [3-6], but TNF-alpha-null mice exhibited no apparent cognitive or e

149 igs during the acute phase of infection, but TNF-alpha-specific CD8(+) T-cell responses increased dur

150 ion and cell inflammatory response caused by TNF-alpha.

151 The production of CCL11 and CCL5 by TNF-alpha was insensitive to both fluticasone and dexame

152 Induction of miR-155 was driven by TNF-alpha, the effect of which was significantly enhance

153 sTNF is generated by TNF-alpha converting enzyme (TACE) proteolytic release o

154 icated activation of pulmonary macrophage by TNF-alpha and/or MCP-1 in the mechanisms of RSV-induced

155 However, CD40 did not cause TNF-alpha or IL-1beta secretion in Muller cells.

156 r and gene activation in response to chronic TNF-alpha signaling.

157 dings establish a mechanism by which chronic TNF-alpha signaling orchestrates a functional interplay

158 nd DSS-induced colitis and increased colonic TNF-alpha, CXCL10, and chemokine (C-C motif) ligand 2 (C

159 Relative colonic TNF-alpha and IL-1beta mRNA levels were calculated.

160 ed upregulation of pro-inflammatory cytokine TNF-alpha in an ImI concentration-dependent manner from

161 able to dose dependently stimulate cytokine TNF-alpha, IL-1beta, IL-6, IL-10, and IL-12 production i

162 ce and presence of an inflammatory cytokine (TNF-alpha) and a well-known cell proliferation inhibitor

163 y and secretion of proinflammatory cytokines TNF-alpha and IL-6.

164 e higher levels of proinflammatory cytokines TNF-alpha, IFN-gamma, IL-2, and IL-17.

165 se (COX)-2 and the proinflammatory cytokines TNF-alpha, IL-6, and IL-12.

166 ter increases in levels of plasma cytokines (TNF-alpha, IL-1beta, IL-6, and IL-10), and greater incre

167 concerted production of three key cytokines: TNF-alpha, IFN-gamma, and IL-2.

168 n of TNF receptor (TNFR)-1 and -2, decreased TNF-alpha-induced phosphorylation of IKKalpha/beta and I

169 Most prominently, glia-derived TNF-alpha has been shown to regulate homeostatic synapti

170 on is mediated by CX3CR1(+) monocyte-derived TNF-alpha.

171 a/FNAB/PMMA/Au reveal that system can detect TNF-alpha in 100pg/ml to 100ng/ml range with high sensit

172 ates atrophy induced by dexamethasone (Dex), TNF-alpha and H2O2 treatment.

173 degranulation and cytokine production (i.e., TNF-alpha and IFN-gamma) against EBV-infected cells, enh

174 Furthermore, we found that effective TNF-alpha production is only induced in the presence of

175 This enhanced TNF-alpha-converting enzyme activity significantly incre

176 following the administration of etanercept (TNF-alpha inhibitor; 1 mg Kg(-1)).

177 apoptotic cells, which stimulated excessive TNF-alpha secretion predominantly from dendritic cells.

178 Addition of exogenous TNF-alpha to mouse tracheal epithelial cells was suffici

179 , through the inhibition of Iba1 expression, TNF-alpha release and NO production.

180 , reduced mitochondrial function facilitated TNF-alpha-mediated NF-kappaB luciferase promoter activit

181 ORF12, encoding a soluble decoy receptor for TNF-alpha, delayed the manifestation of behavioral fever

182 our results implicate an important role for TNF-alpha-producing cytotoxic T-cells in mediating the a

183 EMPs were generated from TNF-alpha-stimulated HUVECs and quantified by using flow

184 R8-dependent type II interferon (IFN-gamma), TNF-alpha, and IL-12 in myeloid dendritic cells are of i

185 roduction of protective cytokines IFN-gamma, TNF-alpha, and IL-12, as well as recruitment of NK cells

186 cells, and inflammatory markers (IFN-gamma, TNF-alpha, and IL-17) in mice with dextran sodium sulfat

187 ponses entail the coproduction of IFN-gamma, TNF-alpha, and IL-2.

188 ls of the proinflammatory factors IFN-gamma, TNF-alpha, and inducible NO synthase in the TME merely 4

189 y cytokines and chemokines (IL-6, IFN-gamma, TNF-alpha, CXCL1, and CCL2) and extensive splenic damage

190 of the pro-inflammatory cytokines IFN-gamma, TNF-alpha, IL-1beta and RANTES and activation of p38/Sta

191 ibroblasts, demonstrating that the IFN-gamma/TNF-alpha/miR-155/PD-L1 pathway is not restricted to HDL

192 educed the expression of inflammatory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6, and CCL2 mRNAs), a

193 of repeated LPS stimulation in vivo, hepatic TNF-alpha and PCNA responses subsided in Nox4-deficient

194 tory responses (lower IL-10 and CCL2, higher TNF-alpha, IL-6, and IL-1beta) toward pathogenic stimuli

195 ld WT (not Arg-II(-/-)) mice contains higher TNF-alpha levels than the young mice and stimulates beta

196 e marrow-derived macrophages produced higher TNF-alpha compared with CD44(-/-) macrophages following

197 though no effect was observed on hippocampal TNF-alpha levels after 1 h of IMM stress, a single BHB p

198 e BHB pre-administration reduced hippocampal TNF-alpha.

199 romoted mucosal secretion of IL-22 and ICOSL/TNF-alpha-dependent release of the IL-22 inducible antim

200 oA led to increased expression of CCL2, IL6, TNF-alpha, and CXCL10 in NCM460-NK-1R cells on SP stimul

201 , and TGF-beta, despite a gradual decline in TNF-alpha expression and macrophage infiltration.

202 mpounds 3a, 6b and 7c and found decreases in TNF-alpha and IL-6 release and increase in IL-1beta.

203 her these changes were due to an increase in TNF-alpha.

204 irculating inflammatory cytokines, including TNF-alpha, IFN-gamma, IL-6, and CCL2.

205 ency in endothelial autophagy also increased TNF-alpha-induced inflammation under high-SS conditions

206 hibitor were protected from diabetes-induced TNF-alpha, IL-1beta, ICAM-1, and NOS2 upregulation.

207 Nox4 silencing suppressed LPS-induced TNF-alpha and PCNA increases in human cells.

208 NF146 caused hypersensitivity to LPS-induced TNF-alpha production in vivo.

209 HA dose-dependently inhibited TLR2-induced TNF-alpha production by murine bone marrow-derived macro

210 We found that AICAR inhibited TNF-alpha-induced CFB expression in ARPE-19 and human pr

211 SseK proteins also inhibited TNF-alpha-induced cell death during macrophage infection

212 Wnt/beta-catenin activity and also inhibits TNF-alpha production and IkappaB degradation in a dose-d

213 Instead, monocyte-derived innate TNF-alpha and inducible NO synthase-producing DCs domina

214 f proinflammatory cytokines, including iNOS, TNF-alpha, and IL-6.

215 Interestingly, TNF-alpha-induced NFkappaB pathway activation was revers

216 croptosis induced by death receptors ligands TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related

217 expressed IL-10R, CD206, and CCR2 but little TNF-alpha or CX3CR1.

218 n OAs, which could be due to increased local TNF-alpha levels, might lead to impaired eosinophil reso

219 We demonstrate that LPS, TNF-alpha, and viral infection, all of which induce robu

220 GPx levels in cord blood as well as maternal TNF-alpha levels were inversely associated with maternal

221 that NKG2D signaling is critical for maximal TNF-alpha release by NK cells.

222 ncreases the activity of the metalloprotease TNF-alpha-converting enzyme.

223 n both unadjusted and fully adjusted models: TNF-alpha: hazard ratios (HRs)(1 pg/ml increments), 1.24

224 inhibition of the anti-inflammatory molecule TNF-alpha-induced protein 3 (TNFAIP3)/A20 in memory CD4(

225 t tertile reported higher risk of mortality: TNF-alpha: HR, 1.45; 95% CI, 1.01-2.09; IL6: HR, 1.55; 9

226 However, neither TNF-alpha gene deletion nor anti-TNF-alpha neutralizing

227 ipt and protein analysis of IFN-gamma and of TNF-alpha and IL-2 revealed that T cell responses consis

228 were no differences in the concentration of TNF-alpha, IL-1beta, IL-6, and IL-8.

229 IL-6-related pathways and downregulation of TNF-alpha upstream elements.

230 e involved in ICAM-1-dependent expression of TNF-alpha in cerebral and dermal MVECs, and CXCL8, CCL3,

231 hild with HIVAN led to the identification of TNF-alpha as a possible mediator of HIV-1 infection.

232 WT and associated with an early increase of TNF-alpha and, later, of IL-10.

233 ted significantly lower expression levels of TNF-alpha (P = .01), IL-1beta (P = .0015), IL-6 (P = .00

234 n coinfected with HIV-1 had higher levels of TNF-alpha and IL-1beta than HIV-uninfected children with

235 lesion volume, and brain cortical levels of TNF-alpha and IL-6.

236 Increased levels of TNF-alpha and IL6 are associated with inflammation and c

237 whereas there was no difference in levels of TNF-alpha or IL-6.

238 rboring R753Q TLR2 expressed lower levels of TNF-alpha, IL-1beta, IL-6, and IL-10 compared with cells

239 ho died in the hospital had higher levels of TNF-alpha, IL-1beta, interleukin 12p70; CCL2, CCL4, CCL1

240 Upon LPS challenge, serum levels of TNF-alpha, KC, IL-6, and IL-10 were significantly increa

241 Neutralization of TNF-alpha normalized neurodevelopmental abnormalities in

242 roduction of IL-12 and IFN-gamma, but not of TNF-alpha, IL-6, and IL-8 upon subsequent infection with

243 itutively active Lyn inhibited production of TNF-alpha and CCL5/RANTES cytokines and down-regulated t

244 -IL-1beta while inhibiting the production of TNF-alpha.

245 p-regulated the expression and production of TNF-alpha.

246 n macrophages also caused down regulation of TNF-alpha production by the macrophages, indicating a co

247 ivity significantly increases the release of TNF-alpha and UL16 binding protein from the surface of t

248 infection, without affecting the release of TNF-alpha, and indicated a role for the inflammasome sen

249 L significantly downregulated the release of TNF-alpha, but showed a lesser effect on IL-8 secretion

250 ing protein capable of inducing secretion of TNF-alpha by a monocyte/macrophage cell line and primary

251 In contrast, supplementation of TNF-alpha and IL-1beta, widely studied proinflammatory c

252 of AMPK, ZMP, did not reverse the effects on TNF-alpha-induced CFB expression, suggesting AMPK-indepe

253 because of the inhibiting effect of PGE2 on TNF-alpha production.

254 A and RvD5n-3 DPA reduced cell adhesion onto TNF-alpha-activated human endothelial monolayers.

255 ndii invaded but did not induce IFN-alpha or TNF-alpha in human pDC.

256 pDCs expressing Tim-3 produced IFN-alpha or TNF-alpha in response to the TLR7 agonists imiquimod and

257 ction was inhibited by anti-IFN-gamma and/or TNF-alpha antibody.

258 ytokine production was mediated by paracrine TNF-alpha-TNFR1 signaling rather than direct ligand sens

259 (N-terminal pro-B-type natriuretic peptide), TNF-alpha, IL-6, IL-12, IL-17, malondialdehyde, and fetu

260 who did not die during the follow-up period (TNF-alpha: median, 1.92 pg/mL; interquartile range [IQR]

261 irst time, a distinctive role for peripheral TNF-alpha in the modulation of the amyloid phenotype in

262 demonstrate that manipulation of peripheral TNF-alpha in the context of arthritis modulates the amyl

263 ich had a differentiated effector phenotype (TNF-alpha-only TEFF), and the level of CD27 expression o

264 sociated Arg-II upregulation, which promotes TNF-alpha release through p38 MAPK leading to beta-cell

265 that plays an essential role in propagating TNF-alpha-mediated signaling pathways.

266 reatment with glycerophosphoinositol reduced TNF-alpha synthesis, which supports the concept that gly

267 reased local/systemic inflammatory response (TNF-alpha downward arrow, IL-1beta downward arrow, IL-6

268 lated factors (i.e., rapamycin, resveratrol, TNF-alpha, and staurosporine), quantitative real-time PC

269 e middle tertile had similar mortality risk (TNF-alpha: HR, 1.09; 95% CI, 0.74-1.61; IL6: HR, 1.05; 9

270 ers stimulated gammadelta T cells to secrete TNF-alpha in response to a variety of tumor cells more e

271 Higher serum TNF-alpha and IL6 levels were associated with higher mor

272 Median serum TNF-alpha and IL6 concentrations were significantly high

273 revalent kidney transplant recipients, serum TNF-alpha and IL6 were independently associated with dea

274 Compared with patients whose serum TNF-alpha or IL6 levels were in the lowest tertile, thos

275 vels of inflammatory cytokines in the serum (TNF-alpha, IL-6, IL-12, TGF-beta, and VEGF) were down re

276 evelopment: SMYD2/IL-6/STAT3/SMYD2 and SMYD2/TNF-alpha/NF-kappaB/SMYD2.

277 he central mediator of inflammation, soluble TNF-alpha (sTNF).

278 y expressed SseK1, SseK2, and SseK3 suppress TNF-alpha-induced, but not Toll-like receptor 4- or inte

279 naling and TNF-alpha production by targeting TNF alpha-induced protein 3 (TNFAIP3).

280 nary, arterial, and myocardial function than TNF-alpha inhibition or cyclosporine treatment.

281 f the JCI, McGeough et al. demonstrated that TNF-alpha, in addition to IL-1beta, plays an important r

282 Furthermore, we found that TNF-alpha enhanced NF-kappaB activation and integration

283 These results indicate that TNF-alpha is a major component of the inflammatory respo

284 We show that TNF-alpha, but not IL-1beta or LPS, promoted nuclear enr

285 The TNF-alpha-only TEFF signature was significantly higher i

286 1 out of 41 indole derivatives inhibited the TNF-alpha effect.

287 Acute administration of the TNF-alpha inhibitor etanercept inhibits carbon tetrachlo

288 ntributed to identify important roles of the TNF-alpha ligand Eiger and mitogenic molecules in mediat

289 9-fold (P < 0.01) via NF-kappaB compared to TNF-alpha-treated control.

290 ticipates in the proinflammatory response to TNF-alpha, therapeutic strategies targeting this transcr

291 letion blunted ROS production in response to TNF-alpha.

292 ls producing mutant UMOD were susceptible to TNF-alpha- and TRAIL-mediated apoptosis due to increased

293 metic compounds (SMCs), sensitize tumours to TNF-alpha-induced killing while simultaneously blocking

294 ifferent dimensions, which are released upon TNF-alpha stimulation of endothelial cell cultures.

295 In vitro studies using TNF-alpha and IL-17A were conducted to dissect basement

296 Our aim was to determine whether TNF-alpha blockade has a beneficial effect on endothelia

297 ontrol macrophages following incubation with TNF-alpha.

298 Stimulation of pulmonary macrophages with TNF-alpha and/or MCP-1 induced expression of both IFN-ga

299 ab or adalimumab, alone or preincubated with TNF-alpha.

300 and CXCL3 TonEBP acted synergistically with TNF-alpha and LPS to induce CXCL1-proximal promoter acti