ライフサイエンスコーパス: TNF-alpha

1 TNF-alpha also triggers SARM1-dependent axon degeneratio

2 TNF-alpha and IFN-gamma caused a lethal cytokine shock i

3 TNF-alpha and IL-10 discriminated between patients with

4 TNF-alpha did not destabilize the Fbxl2 transcript (half

5 TNF-alpha is responsible for accelerated Mtb growth, and

6 TNF-alpha mediated dysregulation in the plasticity of mo

7 TNF-alpha plays a pivotal role in the LPS-upregulated as

8 TNF-alpha production in response to C. albicans hyphae w

9 TNF-alpha rapidly induces co-occupancy of KDM7A and UTX

10 TNF-alpha, via activation of JNK, mediated phosphorylati

11 TNF-alpha- and STS-induced acetylation of H3 and H4 hist

12 TNF-alpha-induced phosphorylation of JNK, p38 and NF-kap

13 antly decreased after chelation (p < 0.001); TNF-alpha decreased from 371.6 +/- 211.3 to 215.8 +/- 14

14 s (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG) was determined by reve

15 ry cytokines and chemokines, including IL-1, TNF-alpha, IL-9, CXCL1, CCL2, and CCL5 in the bronchoalv

16 forming growth factor beta1), interleukin-1, TNF-alpha, and BDNF signaling pathways.

17 has been marked by elevation of IL-6, IL-10, TNF-alpha, and other cytokines and severe CD4(+) and CD8

18 ated H3K4 and H3K27 trimethylation at IL-12, TNF-alpha, and arginase-1 promoters, respectively, where

19 T(h)1 differentiation and expression (IL-12, TNF-alpha, IFN-gamma) were enhanced in the neutrophilic

20 tion of profibrotic T cell cytokines (IL-17, TNF-alpha, IL-9, and IFN-gamma) and chemokine receptors

21 igher levels of MHC II, IFN-gamma, IL-1beta, TNF-alpha, and cathepsin S (Ctss) mRNA transcripts, and

22 d levels of proinflammatory T-bet, IL-1beta, TNF-alpha, and IFN-gamma as assessed on day 3 posttransp

23 The LPS-induced serum levels of IL-1beta, TNF-alpha, and IL-6 were significantly elevated in DUSP1

24 were less capable of expression of IL-1beta, TNF-alpha, IL-6, and IL-12 at baseline and/or following

25 egulates proinflammatory cytokines IL-1beta, TNF-alpha, IL-6, and IL-8 at a similar efficacy to dexam

26 AP group, a significant increase of Notch 2, TNF-alpha, IL-17 and RANKL and a significant decrease of

27 mediators such as type I interferons, IL-6, TNF-alpha or IL-1beta in response to RSV.

28 cterized by elevated concentrations of IL-6, TNF-alpha, and C-reactive protein, which has been termed

29 nse, and reduces circulating IL-1beta, IL-6, TNF-alpha, and IFN-gamma levels in response to Mtb infec

30 stment for biomarkers of inflammation (IL-6, TNF-alpha, high-sensitivity C-reactive protein, fibrinog

31 trials targeting one of 7 mechanisms (IL-6, TNF-alpha, IL-12/23, CD20, COX2, BLgammaS, p38/MAPK14).

32 ficantly upregulated for IFN-y (ratio 1.73), TNF-alpha (ratio 2.05), IL-1beta (ratio 1.45), IL-10 (ra

33 uced TNF-alpha, we examined the effects of a TNF-alpha neutralizing antibody and recombinant TNF-alph

34 Using a TNF-alpha-induced TMJ inflammatory arthritis mouse model

35 underlying mechanism leading to the abnormal TNF-alpha expression in ovarian cancer remains poorly un

36 Following LPS-mediated TLR2/4 activation, TNF-alpha and IL-1beta self-regulated and modulated the

37 ess pronounced during proliferation or after TNF-alpha exposure.

38 VCAM1 transcription in the population after TNF-alpha stimulation.

39 ibit heterogeneous expression of VCAM1 after TNF-alpha stimulation.

40 reating with neutralizing antibodies against TNF-alpha and IFN-gamma protected mice from mortality du

41 Polyclonal antibodies against TNF-alpha suppressed TLR2/4-mediated upregulation of ast

42 d production of tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta).

43 d expression of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) mRNAs, as well as IF

44 conditions but tumor necrosis factor alpha (TNF-alpha) and PKCdelta-i had a significantly higher imp

45 -kappaB such as tumor necrosis factor alpha (TNF-alpha) and vgRNA failed to induce NF-kappaB-dependen

46 s inflamed with tumor necrosis factor alpha (TNF-alpha) by reducing expression of adhesion molecules.

47 IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) from ILC3; and an increase in the levels of C

48 , inhibitors to tumor necrosis factor alpha (TNF-alpha) include etanercept, adalimumab, certolizumab,

49 decreased both tumor necrosis factor alpha (TNF-alpha) mRNA levels and protein levels in comparison

50 treatment with tumor necrosis factor alpha (TNF-alpha) or the strong oxidant pervanadate leads to lo

51 (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production.

52 TLR2-dependent tumor necrosis factor alpha (TNF-alpha) release from bone marrow macrophages, and bot

53 orter following tumor necrosis factor alpha (TNF-alpha) stimulation, confirming the immune-antagonist

54 n 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were also evaluated.

55 e, we show that tumor necrosis factor alpha (TNF-alpha), a critical cytokine linked to the inflammato

56 eukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and CXCL8, and identified NF-kappaB and ATF-

57 L) 1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and high-sensitivity C-reactive protein (hsC

58 (GCSF), MCP-1, tumor necrosis factor alpha (TNF-alpha), and IgG anti-toxin A in blood and IgA/G anti

59 while IL-1beta, tumor necrosis factor alpha (TNF-alpha), and IL-12 levels were upregulated.

60 (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), as well as a rapid expansion of effector and

61 nes, especially tumor necrosis factor alpha (TNF-alpha), CCL3, CCL4, and CCL20, their HIV-1 reactivat

62 eukin-1 (IL-1), tumor necrosis factor alpha (TNF-alpha), IL-6, IL-12/23, IL-17, IL-4/13, IL-5, immuno

63 IL-1alpha, and tumor necrosis factor alpha (TNF-alpha).

64 ty triggered by tumor necrosis factor alpha (TNF-alpha).

65 22 (IL-22), and tumor necrosis factor alpha (TNF-alpha).

66 e the levels of tumor necrosis factor-alpha (TNF-alpha) and cytokine-induced neutrophil chemoattracta

67 high levels of tumor necrosis factor-alpha (TNF-alpha) and other inflammatory cytokines.

68 raphysiological tumor necrosis factor-alpha (TNF-alpha) boosts glutamatergic transmission, which is e

69 vated levels of Tumor Necrosis Factor-alpha (TNF-alpha) in the eye.

70 n-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the gingival crevicular fluid (GCF).

71 ctor (VEGF) and tumor necrosis factor-alpha (TNF-alpha) may regulate several biological processes rel

72 by increasing tumour necrosis factor-alpha (TNF-alpha) production which then enhances reparative hep

73 In adults, anti-tumor necrosis factor-alpha (TNF-alpha) therapy is associated with progression of lat

74 P < 0.001) for tumor necrosis factor-alpha (TNF-alpha), 7.0-fold (CI, 3.5- to 18.0-fold; P < 0.001)

75 in response to tumor necrosis factor-alpha (TNF-alpha), IL-1beta, Escherichia coli lipopolysaccharid

76 eukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 receptor antagonist (IL-1RA),

77 diators such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleuki

78 ssion levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1beta, and interfer

79 small GTPases, tumour necrosis factor-alpha (TNF-alpha)-induced signalling and prevention of cell dea

80 (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha).

81 he secretion of tumor necrosis factor-alpha (TNF-alpha).

82 [IFN-gamma] and tumor necrosis factor alpha [TNF-alpha]) produced by innate lymphoid cells (ILCs) loc

83 but B. subtilis PGA also elicited IL-10 and TNF-alpha, whereas B. licheniformis PGA elicited all tho

84 and cytokine content (IL-6, IL-8, IL-10, and TNF-alpha), and antioxidant activity of human milk was a

85 increased (IL-1beta, IL-6, IL-8, IL-10, and TNF-alpha).

86 MoLCs can be matured, secrete IL-12p70 and TNF-alpha, and stimulate proliferation and cytokine prod

87 Plasma and BAL IL-4, IL-6, IL-10, IL-13 and TNF-alpha correlated with BAL fungal presence, while pla

88 ed CD4(+) T cells that coproduced IL-17A and TNF-alpha, and blockade of IL-17A partially ameliorated

89 and decreased the expression of IL-1beta and TNF-alpha mRNA transcripts, while decreasing the frequen

90 neered cartilage in response to IL-1beta and TNF-alpha using an in vitro murine induced pluripotent s

91 inflammatory protein 1 beta (MIP-1beta), and TNF-alpha from NK cells.

92 lammatory cytokine (IL-1alpha, IL-1beta, and TNF-alpha) and chemokine (CCL3 and CCL4) production.

93 -inflammatory cytokines (IL-6, IL-1beta, and TNF-alpha) was significantly reduced by the application

94 ction in serum levels of IL-6, IL-1beta, and TNF-alpha, a rapid recovery of circulating T and B cell

95 ed those plus IL-12p70, IL-10, IL-1beta, and TNF-alpha.

96 Both IL-1beta/IL-1Ra and TNF-alpha/IL-10 ratio in Candida hyphae-stimulated PBMCs

97 lammatory markers (IL-6, IL-1beta, COX-2 and TNF-alpha) decreased.

98 0.04), and with reduced CSF IFN-y, IL-2, and TNF-alpha concentrations (11.4 vs. 56.0pg/mL p=0.01; 33.

99 The level of IL-6 and TNF-alpha also increased in irisin lacking mice.

100 activation reducing Mincle-mediated IL-6 and TNF-alpha generation by 80-90%.

101 individuals showed higher levels of IL-6 and TNF-alpha in the gingival fluid (P <0.05).

102 inflammatory pathways that involve IL-6 and TNF-alpha increase susceptibility to infection among ind

103 We propose that serum IL-6 and TNF-alpha levels should be considered in the management

104 GCF IL-6 and TNF-alpha levels were significantly reduced in Group 2 c

105 Our digital assay measures IL-6 and TNF-alpha proteins, gram-negative (GN) and gram-positive

106 hics, and a range of comorbidities, IL-6 and TNF-alpha serum levels remained independent and signific

107 cant decrease in GCF and serum LRG, IL-6 and TNF-alpha was detected after periodontal treatment compa

108 LRG, IL-6 and TNF-alpha were determined by ELISA.

109 GCF and serum LRG, IL-6 and TNF-alpha were significantly higher in periodontitis gro

110 Thus, higher plasma levels of IL-6 and TNF-alpha, but not IL-1RA or TGF-beta, were significantl

111 ory cytokines, including IL-1beta, IL-6, and TNF-alpha, in adulthood.

112 We found that high serum IL-6, IL-8 and TNF-alpha levels at the time of hospitalization were str

113 elevated at presentation, and IL-6, IL-8 and TNF-alpha levels were higher in complicated appendicitis

114 any of the treatments applied while IL-8 and TNF-alpha were reduced at treatments which combined temp

115 ory cytokines IL-1beta, IL-2, IL-6, IL-8 and TNF-alpha, prior to starting with the administration of

116 control joints, while IL-2, IL-6, IL-8, and TNF-alpha concentrations did not differ between groups.

117 cytokines (IFN-gamma, IL-10, IL-6, IL-8, and TNF-alpha) contributed to the analysis.

118 d cardiac fibroblast Smad2/3 activation, and TNF-alpha-induced neutrophil adhesion on the heart endot

119 ght/LyoVec and LPS to evaluate IFN-alpha and TNF-alpha production capacities (RIG-I and TLR4 pathways

120 ) mRNAs, as well as IFN-alpha, IFN-beta, and TNF-alpha mRNA levels induced by Sendai virus infection.

121 , CCL3, CCL4, CCL5, CCL11, G-CSF, GM-CSF and TNF-alpha.

122 IL-1a, IL-1b), chemokines (CCL2, CXCL8), and TNF-alpha, are all significantly elevated, resulting in

123 ressing the antiviral cytokine IFN-gamma and TNF-alpha and the proliferation marker Ki67.

124 IFN-gamma and TNF-alpha ELISpot assays on whole blood and PBMCs were u

125 Additionally, INF-gamma and TNF-alpha release was increased compared with molecules

126 Moreover, release of IFN-gamma and TNF-alpha was significantly increased.

127 8(+) Teff-associated cytokines IFN-gamma and TNF-alpha.

128 ) cells had an expansion of IFN-gamma(-) and TNF-alpha(-) double-negative cells compared with those w

129 luated by intracellular IL-2, IFN-gamma, and TNF-alpha production with IL-21 in CD4 or CD107a, granzy

130 esponses and in particular to IFN-gamma- and TNF-alpha-expressing CD4(+) T cells.

131 responsible for accelerated Mtb growth, and TNF-alpha neutralisation reverses augmented Mtb growth c

132 e antiviral activity of AdrA, type I IFN and TNF-alpha are both required and act synergistically.

133 eam targets CD144, Neuroligin 1 (NLGN1), and TNF-alpha-stimulated gene/protein 6 (TSG-6).

134 IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-alpha), inflammatory cell infiltration (CD3 + T cell

135 GCF VEGF and TNF-alpha levels remained unchanged throughout the study

136 crevicular fluid (GCF) HIF-1alpha, VEGF, and TNF-alpha levels in generalized aggressive periodontitis

137 cal parameters and GCF HIF-1alpha, VEGF, and TNF-alpha levels were significantly higher in G-AgP pati

138 Anti-TNF-alpha therapies appear to provide novel and safer tr

139 formed in 15 patients before commencing anti-TNF-alpha therapy but only identified 1 LTBI case; 13 pa

140 8 years who developed TB disease during anti-TNF-alpha therapy.

141 itting infliximab (IFX), an immunogenic anti-TNF-alpha chimeric Ab, to heat stress.

142 chieved-an observation that was lost in anti-TNF-alpha-treated IFNAR(-/-) animals.

143 TNF-alpha activity with a neutralizing anti-TNF-alpha antibody occludes the boost in amplitude of gl

144 Children on anti-TNF-alpha therapy are prone to severe TB disease and sig

145 The median interval between starting anti-TNF-alpha therapy and TB diagnosis was 13.1 (IQR, 7.1-20

146 animals were additionally treated with anti-TNF-alpha (Enbrel).

147 ed mice indicate that NPSCs loaded with anti-TNF-alpha siRNA cause changes to the lipid composition i

148 es in downstream signalling elements such as TNF-alpha and ICAM-1.

149 ction of pro-inflammatory mediators, such as TNF-alpha and IL-6.

150 Although the roles of cytokines such as TNF-alpha, IL-12, IFN-gamma, and IL-10 in immunity and p

151 ts, TLR2, TLR3, or TLR4 agonists, as well as TNF-alpha, IL-6, or IL-17A, but not IFN-gamma, similarly

152 activity of ADAM17, the membrane-associated TNF-alpha-converting enzyme.

153 rmore uncover increased interactions between TNF-alpha-induced super enhancers at NF-kappaB-relevant

154 We also found that blood TNF-alpha and CXCL13 concentrations are significantly co

155 relation was found between IL-1beta and both TNF-alpha and IL-6.

156 The LrS attenuated both TNF-alpha- and STS-induced gene expression involved in N

157 w that in primary human CD4(+) T cells, both TNF-alpha(+) and IL-2(+) vesicles can tether with endocy

158 ssion and suppresses LTP by increasing brain TNF-alpha concentrations, directly linking microglia to

159 d, based on pathways known to be affected by TNF-alpha, whereas NPSCs loaded with scrambled siRNA do

160 on capacity was almost completely blocked by TNF-alpha neutralization alone.

161 nges in the monocytes/macrophages induced by TNF-alpha.

162 Blocking urethane-induced inflammation by TNF-alpha neutralization inhibited tumorigenesis and rev

163 ne target during inflammatory stimulation by TNF-alpha in skeletal muscle.

164 In contrast, TNF-alpha inhibition did not affect LPA-dependent cell p

165 , IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamma, GM-CSF, MIP-1alpha, and Eotaxin-1

166 antibodies against the inflammatory cytokine TNF-alpha.

167 n-regulation of the proinflammatory cytokine TNF-alpha in the hippocampus.

168 ulation by a major proinflammatory cytokine, TNF-alpha, regulates skeletal myogenesis by inhibiting t

169 ion increased the pro-inflammatory cytokines TNF-alpha, IFN-gamma, and IL-2 more than the anti-inflam

170 u/Zn-SOD and GPx-4), inflammatory cytokines (TNF-alpha and TGF-beta1), lipid metabolism (FASN and CYP

171 n by suppressing pro-inflammatory cytokines (TNF-alpha, IL-1beta, CCL-3 and IL-6), and reduced oxidat

172 sed the levels of proinflammatory cytokines (TNF-alpha and IL-1beta), oxidative stress (MDA and OSI),

173 pha2a, IFN-gamma, proinflammatory cytokines (TNF-alpha, IL-2, IL-12p70), and chemokines (CXCL10, C-C

174 e upregulation of proinflammatory cytokines (TNF-alpha, IL-6, and IL-1beta) that are associated with

175 sponders showed significantly more decreased TNF-alpha levels compared with nonresponders (P = 0.046)

176 the mediators driving the network differed: TNF-alpha, IL-1beta, and IL-6 predominated in WT mice, w

177 In vitro, TGFbeta1-mim downregulated TNF-alpha production, IL-8 gene expression, and cytokine

178 periodontitis donor, stimulation with either TNF-alpha, IL-1beta, Ec-LPS, or Pg-LPS, increased the se

179 LPA enhanced TNF-alpha mRNA through NF-kappaB-mediated transcriptiona

180 of PD-1 accelerates Mtb growth via excessive TNF-alpha secretion.

181 issue that produced IFN-gamma also expressed TNF-alpha and IL-22.

182 MG-hBORGs, releasing tumor necrosis factor (TNF-alpha) and interleukin-1 (IL-1beta) and thereby mimi

183 ould down-regulate pro-inflammatory factors (TNF-alpha, IL-1beta, and IL-6) and up-regulate an anti-i

184 iet had a reduction in inflammatory factors (TNF-alpha, IL-1beta, IL-5) and suppressive immune popula

185 Pericardial fat TNF-alpha expression was upregulated in PCSK9-HFD, coloc

186 +) T(H1) cells and aberrant extra-follicular TNF-alpha accumulation.

187 tent with increased CR3 expression following TNF-alpha priming, production of reactive oxygen species

188 P < 0.001) for IL-2, with no difference for TNF-alpha or CD107a.

189 Recently, we found TNF-alpha upregulated MHC-II in AT-II in vitro.

190 and inhibited inflammatory mediators (e.g., TNF-alpha and CCL5).

191 ines are delivered multidirectionally (e.g., TNF-alpha).

192 while the CD68(+) macrophage, IFN-gamma(+), TNF-alpha(+), and iNOS(+) immunolabeling fractions incre

193 trast, the CD68(+) macrophage, IFN-gamma(+), TNF-alpha(+), and iNOS(+) immunolabeling fractions incre

194 riminated high responders (G-CSF, IFN-gamma, TNF-alpha) correlated with both egress of circulating vi

195 The release of IFN-gamma, TNF-alpha, IL-2, IL-4, IL-6, IL-10 and IL-17A from isola

196 The expression of IFN-gamma/TNF-alpha by ILCs and NK cells combined likely triggers

197 Concentration distributions for IL-6, GCSF, TNF-alpha, and IgG anti-toxin A in blood, as well as IgA

198 and upregulation of pro-inflammatory genes (TNF-alpha, IL-1beta and Cxcl-1) and also apoptosis of ep

199 In a neuroinflammatory model of glaucoma, TNF-alpha induces SARM1-dependent axon degeneration, oli

200 >=1000 copies/mL was associated with higher TNF-alpha levels (P = .013).

201 al microvascular endothelial cells (HRMECs), TNF-alpha stimulation causes increased RUNX1 expression,

202 ay inhibitors, we determined that in HRMECs, TNF-alpha-induced RUNX1 expression occurs via JNK activa

203 wo, growth factors, human IL-1beta and human TNF-alpha, from an individual droplet of embryo culture

204 ith change in SBP, but not in renal hypoxia, TNF-alpha levels, or renal function.

205 g expansion in an MHC-II-dependent manner in TNF-alpha-mediated IDLA.

206 At week 52, reductions in TNF-alpha (P= 0.0063) and ferritin (P= 0.0354), and an i

207 The silencing of MCL and Mincle resulted in TNF-alpha secretions similar to that of macrophages trea

208 or)adrenaline-exposed cells showed increased TNF-alpha (tumor necrosis factor-alpha) production.

209 Chemerin/ChemR23 induced TNF-alpha and IL-6 expression dependent on Erk1/2, p38 M

210 plore the biological outcomes of LPA-induced TNF-alpha, we examined the effects of a TNF-alpha neutra

211 knockout screen that identified LPS-induced TNF-alpha factor (LITAF) as the HBL receptor.

212 Pro-inflammatory (TNF-alpha, IL-6) and pro-fibrotic (TGF-beta1) cytokines

213 que psoriasis include biologics that inhibit TNF-alpha, p40IL-12/23, IL-17, and p19IL-23, as well as

214 er mean IL-1beta (P = .005), 40% higher mean TNF-alpha (P < .001), and 27% higher mean hsCRP (P = .00

215 idated that a cell-based assay that measures TNF-alpha production by CD14(+)16(+) intermediate monocy

216 Mechanistically, TNF-alpha and IFN-gamma co-treatment activated the JAK/S

217 esponse to LPA, indicating that LPA-mediated TNF-alpha production relies on both transcriptional upre

218 nd that the prominence of intra-graft memory TNF-alpha and IL-17 double-positive T helper type 17 (Th

219 23 effectively reduces neutrophil migration, TNF-alpha secretion, and tissue inflammation in mice (fe

220 LPS-induced release of IL-1beta but not TNF-alpha was further found greatly inhibited in the CNS

221 s (ECs), where they are regulated by a novel TNF-alpha-responsive microRNA, miR-3679-5p.

222 ase is due to acute and reversible action of TNF-alpha and is not associated with increased human-Abe

223 cts that can be attributed to alterations of TNF-alpha-dependent signalling pathways and defects in v

224 Blockade of TNF-alpha signaling significantly reduced the production

225 ction, we found that only the combination of TNF-alpha and IFN-gamma induced inflammatory cell death

226 eatures, we found that the concentrations of TNF-alpha change little from day 3 to day 5-6, but the c

227 ts present increased brain concentrations of TNF-alpha, augmented glutamatergic transmission, suppres

228 in vitro effect of RSV on various effect of TNF-alpha, a major proinflammatory cytokine for periodon

229 3 [0.2-4.5]) and a higher gene expression of TNF-alpha and IL-10 at 45I-120R.

230 arian cancer patients, induced expression of TNF-alpha mRNA and release of TNF-alpha protein in ovari

231 bioactive lipid LPA drives the expression of TNF-alpha to regulate an inflammatory network in ovarian

232 We identified reduced generation of TNF-alpha in lesions of MyD88-deficient animals, a pro-i

233 er biological responses to LPA, induction of TNF-alpha by LPA also depended on the transactivation of

234 treatment significantly decreased levels of TNF-alpha (Hedge's g = 0.60; 95%CI, 0.26-0.94; P = 0.000

235 RB1 allele lead to increased serum levels of TNF-alpha and anticitrullinated cyclic peptide Abs, alon

236 Low levels of TNF-alpha and IL-10 and high levels of CCL22 predicted b

237 SPS increased the serum levels of TNF-alpha and IL-1beta.

238 addition, these cells express high levels of TNF-alpha and IL-2, and provide B cell help for IgG prod

239 sodes of asthma-like symptoms, and levels of TNF-alpha, CCL22, and IL-10 may predict the response to

240 and CRP and both mRNA and protein levels of TNF-alpha.

241 proinflammatory gene expression pathways of TNF-alpha, NF-kappaB, and IFN-beta.

242 al the AD-modifying therapeutic potential of TNF-alpha inhibition in the central nervous system.

243 d CD86 molecules and increased production of TNF-alpha and IL-1beta.

244 deficiency results in reduced production of TNF-alpha, IL-6, and IL-1beta and in limited M1 macropha

245 ocyte phenotype with decreased production of TNF-alpha, IL-6, IL-12p70, IL-10, GM-CSF, VEGF, MIP-1bet

246 enuated by the LrS, as was the production of TNF-alpha- and STS-induced proinflammatory cytokines and

247 Acute reduction of TNF-alpha activity with a neutralizing anti-TNF-alpha an

248 expression of TNF-alpha mRNA and release of TNF-alpha protein in ovarian cancer cells.

249 n, supporting an autocrine/paracrine role of TNF-alpha on astrocyte proliferation.

250 o diffusive rather than localized effects on TNF-alpha production.

251 obacillus rhamnosus R0011 secretome (LrS) on TNF-alpha and Salmonella enterica subsp. enterica serova

252 both cytokines or exclusively to IL-1beta or TNF-alpha.

253 Suppression of either IFN-alpha or TNF-alpha production capacity was associated with longer

254 n added alone, or in combination with LPS or TNF-alpha in ASM.

255 roup 2 compared to control (P(IL-6) =0.01, P(TNF-alpha) =0.02).

256 )] and tumor necrosis factor alpha-positive [TNF-alpha(+)]), and effector molecule (inducible nitric

257 tion marker (IL-6, CRP [C-reactive protein], TNF-alpha R1, D-dimer, and fibrinogen).

258 In human TB, pulmonary TNF-alpha immunoreactivity is increased and circulating

259 -alpha neutralizing antibody and recombinant TNF-alpha soluble receptor on LPA-stimulated expression

260 rginine deiminase 4 (PAD4) inhibitor reduced TNF-alpha and IL-6 compared to WT neutrophils treated wi

261 937 or THP-1 cells, the mNLS variant reduced TNF-alpha or IFN-beta mRNA expression to a similar exten

262 adhesion to endothelium, as well as reducing TNF-alpha, IL-1beta, COX2 expression in macrophages.

263 variant (223Q) maintain activity in reducing TNF-alpha induction during M. pneumoniae infection.

264 revented ovarian cancer cells from releasing TNF-alpha protein in response to LPA, indicating that LP

265 We found that noise induced more robust TNF-alpha expression in C57BL/6 than in FVB mice.

266 mined periodontal tissue cathepsin K, Runx2, TNF-alpha, and IL-6 expression.

267 ion of caspase-8, TNFR1, and increased serum TNF-alpha.

268 n partially attenuated the increase of serum TNF-alpha.

269 ith interactions being present in Cu/Zn-SOD, TNF-alpha, TGF-beta1, FASN and IGF-I.

270 LL-CFA/I treatment suppressed splenic TNF-alpha(+)CD8(+) T cells 6-fold at 11 weeks (p < 0.005

271 expression negatively correlates with sputum TNF-alpha concentrations.

272 At the pro-tumor inflammatory stage, TNF-alpha-dependent lung inflammation plays an important

273 hermore, at the pro-IDLA inflammatory stage, TNF-alpha-neutralization or CXCR-2 deficiency inhibited

274 TMA and cadaverine inhibited LPS-stimulated TNF-alpha and IL-6 secretion by primary human monocytes.

275 tic effects, possibly by inhibiting systemic TNF-alpha.

276 nes, methotrexate, cyclosporine, tacrolimus, TNF-alpha antagonists, vedolizumab, tofacitnib, or ustek

277 Clinical protocols targeting TNF-alpha, IL-17, and Th17 warrant further testing.

278 MCN undergoes constitutive cleavage and that TNF-alpha treatment dramatically increases this cleavage

279 footprint from the naive monocyte, and that TNF-alpha was the most sensitive cytokine or chemokine i

280 We found that TNF-alpha and IL-10 control optimal CXCL13 gene expressi

281 rtic endothelial cells (HAoECs) we show that TNF-alpha, a known risk factor for endothelial dysfuncti

282 We previously showed that TNF-alpha blockade during T cell stimulation in CD4(+) T

283 elated in patients with IPF, suggesting that TNF-alpha contributes to CXCL13 production in humans.

284 RNA) against SMPD3 results in defects in the TNF-alpha mediated expression of CD11c.

285 eutrophil adhesion and transmigration in the TNF-alpha-inflamed cremaster muscle and a prolongation o

286 We found that RSV notably inhibited the TNF-alpha-induced osteoclast formation, endothelial cell

287 Moreover, the TNF-alpha, IL-17A, and IL-22-induced phosphorylation of

288 on both transcriptional upregulations of the TNF-alpha gene and the activity of ADAM17, the membrane-

289 Here we show that the TIPE (TNF-alpha-induced protein 8-like) family of proteins pil

290 Although a role for TNFSF2 (TNF-alpha) cannot be ruled out, transcriptomics suggest

291 n patients with or without prior exposure to TNF-alpha antagonists, (2) comparative efficacy and safe

292 Using TNF-alpha pathway inhibitors, we determined that in HRME

293 oid cell-mediated inflammatory responses via TNF-alpha, which are essential for phagocytic myelin deb

294 ulations are a significant source of ex vivo TNF-alpha production.

295 In this study, we explored whether TNF-alpha-mediated inflammation upregulates MHC-II on AT

296 intestinal epithelial cells challenged with TNF-alpha or STS.

297 se individuals and positively corelated with TNF-alpha gene expression.

298 increased after priming the endothelium with TNF-alpha, our data suggests that this mechanism could p

299 reatment of patient-derived fibroblasts with TNF-alpha resulted in reduced phosphorylation of the ext

300 Additionally, stimulation with TNF-alpha and D-glucose had an additive effect on RUNX1