ライフサイエンスコーパス: TNF

1 TNF activates opposing pathways leading to caspase-8-med

2 TNF has been reported to increase entry of HCV pseudopar

3 TNF inhibited completion of the HCV infectious cycle in

4 TNF plays an integral role in inflammatory bowel disease

5 TNF receptor-associated death domain (TRADD) is an essen

6 TNF receptor-associated factor 6 (TRAF6) is identified a

7 TNF was also required during the allergen challenge phas

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

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

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

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

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

13 TNF-related apoptosis-inducing ligand (TRAIL) is a death

14 TNF-related apoptosis-inducing ligand (TRAIL) was initia

15 TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) has

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

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

18 factor NF-kappaB in response to FGF and IL-1/TNF, respectively.

19 6, FOXP3), cytokines (IL-1beta, IL-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismutase, c

20 d with IL-17A (r = 0.74, P < .001) and IL-17/TNF-synergistic/additive gene expression.

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

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

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

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

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

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

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

28 IKK-beta, TNF receptor-associated factor 6, TNF receptor-associated factor 2, receptor-interacting p

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

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

31 a higher false alarm metric in this abnormal TNF signaling system indicates perceiving more cytokine

32 (66.4%) and/or tumor necrosis factor alpha (TNF-alpha) (63.7%).

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

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

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

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

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

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

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

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

44 tenin signalling for the control of PD-1 and TNF receptor proteins.

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

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

47 acrophages, and elevated levels of IL-17 and TNF.

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

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

50 ctional analysis revealed defective IL-2 and TNF production yet retained expression of IFN-gamma and

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

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

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

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

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

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

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

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

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

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

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

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

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

64 iated with increased cytotoxic character and TNF and IFNgamma production upon target-cell recognition

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

66 n murine enteroids and colonoid cultures and TNF-induced beta-catenin activation in nontransformed hu

67 pressing GBM using a combination of EGFR and TNF inhibition.

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

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

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

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

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

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

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

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

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

77 re collected and analyzed histologically and TNF protein levels measured by enzyme-linked immunosorbe

78 signaling crosstalk between interferons and TNF is integrated at the level of chromatin to reprogram

79 of the TLR and PPAR families, NF-kappaB, and TNF-related weak inducer of apoptosis (TWEAK).

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

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

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

83 tream of NF-kappaB-inducing kinase (NIK) and TNF receptor family members including lymphotoxin-beta r

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

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

86 Anti-TNF treatment, as well as metformin and methotrexate, wh

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

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

89 nti-tumor necrosis factor alpha agents (anti-TNF) in treating cutaneous sarcoidosis is lacking.

90 nt with both immunosuppressant (IS) and anti-TNF before colectomy was independently associated with I

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

92 sease (CD) patients induced by chimeric anti-TNF mAbs.

93 ncrease in postoperative complications, anti-TNF agent use within 90 days of surgery among patients w

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

95 r IBD, and has particular relevance for anti-TNF-resistant patients.

96 y; in FcgammaR(-/-)Rag1(-/-) mice given anti-TNF these numbers were as low as FcgammaR(-/-)Rag1(-/-)

97 To determine the efficacy and safety of anti-TNF in treating cutaneous sarcoidosis in a large observa

98 is strongly associated with failure of anti-TNF therapy.

99 erapy responsiveness or side effects of anti-TNF therapy.

100 In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion

101 , 2.35; 95% CI, 1.31-4.22; P < .001) or anti-TNF monotherapy (aHR, 2.53; 95% CI, 1.35-4.77; P < .001)

102 D, the use of thiopurine monotherapy or anti-TNF monotherapy was associated with a small but statisti

103 Unlike preoperative anti-TNF agent use among patients who underwent colectomy or

104 olons from Rag1(-/-) mice that received anti-TNF had an increased number of CD206(+) macrophages comp

105 lammatory bowel disease (IBD) receiving anti-TNF therapy.

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

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

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

109 is who were refractory or intolerant to anti-TNF drugs and other biological treatments, both dosing r

110 , 0.41-0.67), 32 in patients exposed to anti-TNF monotherapy (IR, 0.41; 95% CI, 0.27-0.55), and 14 in

111 ortunately, not all patients respond to anti-TNF therapy, and some patients show paradoxical immune s

112 owel disease (IBD) who lose response to anti-TNF therapy.

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

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

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

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

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

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

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

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

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

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

123 otein interactions with IKK-alpha, IKK-beta, TNF receptor-associated factor 6, TNF receptor-associate

124 ays, it does not capture the overlap between TNF-induced noisy response curves.

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

126 We demonstrate that both TNF-R and nucleotide-binding oligomerization domain stim

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

128 dium sulfate-induced colitis, ameliorated by TNF inhibition.

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

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

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

132 reases, such as: MMP9 correlated with CCL22, TNF, FASL, RUNX3, and SEMAD4 in AdMSC and, in T cells, M

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

134 e formation of the TNF-R1 signaling complex (TNF-RSC) to mediate downstream cellular fate decision.

135 CRP, TNF, sIL-6R, I-FABP, sCD14, D-dimer, and HA levels were

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

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

138 es showed that the proinflammatory cytokines TNF and type I interferons induced transcriptional casca

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

140 ce were exposed to LPS, and serum cytokines (TNF and IL-10) were measured.

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

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

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

144 sialylation of TNFR1 had no effect on early TNF-induced signaling events, including the rapid activa

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

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

147 Additionally, extended TNF treatment resulted in the selective enrichment of cl

148 process that can be generally boosted by F8-TNF and doxorubicin treatment.

149 ting cytotoxic capacity were increased by F8-TNF plus doxorubicin treatment, arguing that cognate CD8

150 selective splice isoforms of fibronectin (F8-TNF), can be exploited to eradicate sarcomas in immunoco

151 HI-164 fibrosarcoma with a combination of F8-TNF and doxorubicin, curing the majority of treated anim

152 had higher levels of tumor necrosis factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitme

153 ed with at least one tumour necrosis factor (TNF) antagonist (which had failed in 96 [79%]).

154 OUND & AIMS: Although tumor necrosis factor (TNF) antagonists reduce many clinical features of inflam

155 nction in response to tumor necrosis factor (TNF) compared with normal donor EC cultures.

156 The tumor necrosis factor (TNF) family ligand ectodysplasin A (EDA) is produced as

157 Dysregulation of tumor necrosis factor (TNF) receptor signaling is a key feature of various infl

158 e driven by increased tumor necrosis factor (TNF) secretion, which leads to activation in turn of c-J

159 Analysis of tumor necrosis factor (TNF) signaling pathway which regulates the transcription

160 rgistic IFN-gamma and tumor necrosis factor (TNF) stimulation promotes strong activation of brain blo

161 Eiger, the only known tumor necrosis factor (TNF) superfamily homolog in Drosophila, Coxiella-infecte

162 ent assays quantified tumor necrosis factor (TNF), interleukin (IL)-12, and IL-10 in gingival tissues

163 AI and inhibition of tumour necrosis factor (TNF), lipopolysaccharide or polyinosinic:polycytidylic a

164 alpha (PPARGC1A), and tumor necrosis factor (TNF), was changed in adipose tissue by overfeeding.

165 terferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and IL-1beta protein levels.

166 terferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-2, but not IL-17A; iii)

167 h factor (VEGF-A) and tumor necrosis factor (TNF)-alpha levels.

168 and the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 in the syno

169 ne plasticity through tumor necrosis factor (TNF)-alpha-dependent mechanisms.

170 Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known

171 cytokines, including tumor necrosis factor (TNF).

172 Confirming and extending these findings, TNF, IL-2, and IL-21 also synergistically triggered the

173 1 microM), markedly increase (by 1,000-fold) TNF gene expression in cultured human LAD2 and primary m

174 assays, we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type

175 ry, we found that RARgamma was essential for TNF-induced RIP1-initiated apoptosis and necroptosis.

176 Our study uncovers key roles for TNF and, to a lesser extent, IL-17 as mediators of liver

177 omplexes by mediating RIP1 dissociation from TNF receptor 1.

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

179 ctivation, develop cutaneous ulceration from TNF exposure, and exhibit severe dextran sodium sulfate-

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

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

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

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

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

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

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

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

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

189 Here, we show how TNF-linked antibodies, which recognize tumor-selective s

190 cosylated antibodies against mouse and human TNF (adalimumab).

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

192 alse discovery rate < 0.05), including IFNG, TNF, CSF2, chemokines, such as CCL3, CCL4, and XCL1, and

193 nd stimulates cytokine expression (IFNgamma, TNF) by human MAIT cells.

194 tic translation initiation factor 4E axis in TNF production downstream of NOD1.

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

196 were lower, in wild-type DCs (wtDCs) than in TNF knockout (TNFko) DCs.

197 vity by proinflammatory cytokines, including TNF, interferes with bone remodeling during inflammation

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

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

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

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

202 TLR ligands, but not proteases, induced TNF during allergic sensitization.

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

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

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

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

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

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

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

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

211 single injection of picogram amounts of NGR-TNF, a tumor vessel-targeted TNFalpha derivative current

212 or more biological treatments including non-TNF drugs, and 166 (19%) of 878 were not taking a DMARD

213 singly, NK-1 antagonists also inhibit 50% of TNF secretion (P < 0.001) when stimulated only by IL-33,

214 The pro-survival effect of TNF depends on the activity of the TNFR2/TRAF1 pathway t

215 The direct effect of TNF on stem cells was demonstrated by studies of TNF-ind

216 f TRIM28 strikingly suppressed expression of TNF receptor (TNFR)-1 and -2, decreased TNF-alpha-induce

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

218 Injection of TNF greatly increased levels of cell death in intestinal

219 A against Tnf mRNA reduced protein levels of TNF in colon tissues, compared with mice with colitis gi

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

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

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

223 h domain (TRADD) is an essential mediator of TNF receptor signaling, and serves as an adaptor to recr

224 Neutralization of TNF-alpha normalized neurodevelopmental abnormalities in

225 increased I-FABP levels but normalization of TNF, sIL-6R, and D-dimer levels.

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

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

228 portant implications for the pathogenesis of TNF-mediated enteropathies and chronic inflammatory dise

229 s identify a unique amplification process of TNF synthesis and secretion via the interaction of NK-1

230 exhibited significantly higher production of TNF and IFNgamma, elevated natural cytotoxicity, and inc

231 of exhaustion, such as reduced production of TNF and IL2 and expression of coinhibitory receptors.

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

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

234 Furthermore, the TsSP-induced reduction of TNF secretion from DCs is reversed by receptor antagonis

235 found cIAP1 to be required for regulation of TNF-induced intestinal epithelial cell death and surviva

236 ing protein, revealed an enhanced release of TNF in the absence of Fhl2.

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

238 s by impeding the Adam17-mediated release of TNF.

239 appreciated critical cell-autonomous role of TNF on monocytes for their survival, maintenance, and fu

240 on stem cells was demonstrated by studies of TNF-induced Wnt/beta-catenin target gene expression in m

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

242 -TNF-alpha drugs and in the potential use of TNF-targeted therapies for AD.

243 ice revealed that mucosal repair depended on TNF production by BM-derived cells and TNFR expression b

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

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

246 derived cells in mice deficient in IL-17 or TNF.

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

248 This HVEM mutein did not bind CD160 or TNF ligands but did bind BTLA with 10-fold stronger affi

249 we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type counter

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

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

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

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

254 KCa3.1(-/-) reduced RANKL+/-TNF-stimulated phosphorylation of CREB and expression of

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

256 4 (23.7% decrease) and significantly reduced TNF and IL-12 levels in gingival tissues.

257 4 (23.7% decrease) and significantly reduced TNF and IL-12 levels in the gingival tissues.

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

259 with low-dose LPS resulted in elevated serum TNF levels compared with Nlrp3L351P Casp1/11-/- mice and

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

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

262 nercept, a decoy receptor that binds soluble TNF, fails to improve disease.

263 ng/mL) in combination also greatly stimulate TNF secretion (by 4,500-fold).

264 eptor reduction also decreases SP-stimulated TNF secretion by 30% (P < 0.05), suggesting an interacti

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

266 We hypothesized that TNF exerts beneficial effects on intestinal epithelial c

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

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

269 Here we show that TNF-induced activation of MK2 results in global RIPK1 ph

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

271 f MyD88-independent receptors, including the TNF receptor and TLR3.

272 3 complex to the IL-10 promoter, but not the TNF promoter, thereby tipping the balance towards inflam

273 ation is dependent on RANKL, a member of the TNF family of cytokines.

274 Members of the TNF receptor superfamily (TNFRSF) are key costimulators

275 e Item et al. show that Fas, a member of the TNF receptor superfamily, contributes to mitochondrial d

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

277 with TNFalpha leads to the formation of the TNF-R1 signaling complex (TNF-RSC) to mediate downstream

278 Activation of the TNF-RSC is modulated by different types of ubiquitinatio

279 on, or systemic injections of an antibody to TNF before or during sensitization and challenge phase o

280 9-fold (P < 0.01) via NF-kappaB compared to TNF-alpha-treated control.

281 nism that regulates the cellular response to TNF and may promote cancer cell survival within TNF-rich

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

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

284 tinal organoids, died rapidly in response to TNF.

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

286 ukin-1 receptor-associated kinase)1/4-TRAF6 (TNF receptor-associated factor 6), leading to integrin a

287 TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related Apoptosis-Inducing Ligand); is an extremely

288 CE) proteolytic release of the transmembrane TNF (tmTNF) ectodomain.

289 ]arene-C60, bisporphyrin-trinitrofluorenone (TNF), and Hamilton's bis(acetamidopyridinyl)isophthalami

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

291 These findings might help to explain why TNF blockade improves lung function in only some patient

292 urthermore, NOSTRIN interacted directly with TNF receptor-associated factor 6 (TRAF6), leading to the

293 r incubation of crypt-derived enteroids with TNF reduced their expression of DRA messenger RNA and pr

294 When cells were incubated with TNF before infection, the subsequent antiviral effects o

295 C57BL/6 mice were injected with TNF (5 mug/mouse for 3-6 hours) or vehicle (control); in

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

297 Injection of mice with TNF or incubation of crypt-derived enteroids with TNF re

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

299 ce, cultured enteroids, incubated these with TNF (50 ng/mL, 24 hours), and quantified messenger RNAs.

300 and may promote cancer cell survival within TNF-rich tumor microenvironments.