ライフサイエンスコーパス: TNF

1 TNF deficiency did not affect viral load or leukocyte re

2 TNF induces R-Ras upregulation in endothelial cells via

3 TNF plays a key role in immune-mediated inflammatory dis

4 TNF receptor superfamily member 14 (TNFRSF14, also calle

5 TNF signaling through TNFR1 p55 was required for upregul

6 TNF(-/-) mice succumbed to fulminant disease whereas wil

7 TNF-alpha also triggers SARM1-dependent axon degeneratio

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

9 TNF-alpha mediated dysregulation in the plasticity of mo

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

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

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

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 In (LPS/ATP-stimulated) PBMCs, IL-18/TNF/caspase-1 were all significantly decreased and IL-10

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

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

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

25 epatocellular injury and death from IL-1beta/TNF in combination, but neither IL-1beta nor TNF alone.

26 eased hepatocyte autophagy promotes IL-1beta/TNF-induced necrosis from impaired energy homeostasis an

27 subgroups of high (N = 17) and low (N = 55) TNF-KYN/TRP groups.

28 ), cytokines and growth factors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), ATM and p53 signaling pathways

29 tients showed reduced levels of plasma IL-6, TNF, IL-1beta, and phosphorylated STAT3 as well as swift

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

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

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

33 pharmacodynamic activity of compound 42 in a TNF-induced IL-6 mouse model and in vivo activity in a c

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

35 lation, PACRG was recruited to the activated TNF receptor complex and interacted with LUBAC component

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

37 Loss of ADAM17, TNF and the TNF receptor Grindelwald in pigmented glial

38 n a dose-dependent manner, without affecting TNF activity or osteoblast differentiation.

39 eloped infections after treatment (19% after TNF and 17% after immunomodulators) compared with fit pa

40 lators) compared with fit patients (9% after TNF and 7% after immunomodulators; P < .01 for frail vs

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 22 (IL-22), and tumor necrosis factor alpha (TNF-alpha).

58 d by short-term tumor necrosis factor-alpha (TNF) treatment were largely sustained in the FLS exposed

59 tokines such as tumor necrosis factor-alpha (TNF), the master transcriptional regulator nuclear facto

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Serum IL-18 and TNF decreased significantly with treatments, but IL-1bet

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

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

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

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

78 (+) T cells concomitantly producing IL-2 and TNF dominated the responses from vaccinees after each va

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

80 nd cytokine production (IFN-gamma, IL-2, and TNF), with the highest median magnitude detected after t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 ssion levels of GzmB, CD107a, IFN-gamma, and TNF was examined.

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

99 xicity induced by the cytokines IFNgamma and TNF.

100 ory cytokines (IL [interleukin] 1B, IL6, and TNF [tumor necrosis factor]).

101 nflammatory pathways linked to Toll-like and TNF receptor activation and arachidonic acid metabolism

102 MAPK and TNF signaling pathways were the most significantly upreg

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

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

105 Anti-TNF therapy ameliorates disease in many patients with rh

106 d the development of antibodies against anti-TNF agents.

107 red with neutral) faces (p = 0.032) and anti-TNF conversely decreasing right amygdala reactivity (acr

108 a-priori hypothesis, both IFN-alpha and anti-TNF significantly modulated amygdala reactivity with IFN

109 equate suppression of Th17 responses by anti-TNF in nonresponders, and direct targeting of the USF2-s

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

111 Conversely, anti-TNF significantly improved depressive symptoms (Hospital

112 8 years who developed TB disease during anti-TNF-alpha therapy.

113 Anti-tumor necrosis factor (anti-TNF) therapies are the most widely used biologic drugs f

114 Anti-tumor necrosis factor (anti-TNF) therapy resistance is a major clinical challenge in

115 of patients naive to and having failed anti-TNF therapy, respectively, achieving HS clinical respons

116 ients with HS naive to or having failed anti-TNF therapy.

117 predict severe outcome and the need for anti-TNF therapy with a high level of precision.

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

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

120 n subunit mediated the effectiveness of anti-TNF therapy in human immune cells.

121 his cohort, 5% of patients who received anti-TNF therapy and 7% of patients who received an immunomod

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

123 a potential therapeutic approach in the anti-TNF refractory RA.

124 d intestinal cell types contributing to anti-TNF resistance.

125 ypes were associated with resistance to anti-TNF therapy.

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

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

128 grin pathway signaling in patients with anti-TNF-resistant colonic Crohn's disease (cCD) and ulcerati

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

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

131 orthopoxviruses bound to membrane-associated TNF and dampened inflammatory gene expression through re

132 8 secretion induced by heat-killed bacteria, TNF, or latrunculin A.

133 We discover new functional synergies between TNF and IFNbeta controlling dendritic cell-T cell crosst

134 y the clinical success of therapies blocking TNF and IL-23 in IBD and in some forms of SpA.

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

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

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

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

139 ciated with inflammatory responses driven by TNF and Toll-like receptors via NF-kappaB, eicosanoid bi

140 vation, apoptosis and necroptosis induced by TNF.

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

142 protein, possibly generalizable to other C1q/TNF-related proteins (CTRPs) and C1q family members.

143 The C1q complement/TNF-related protein superfamily (CTRPs) displays differe

144 nonical NF-kappaB2 pathway and its component TNF receptor-associated factor 3 (TRAF3) by the VDRA par

145 eurons residing in the brainstem DMN control TNF production, revealing a role for brainstem coordinat

146 oncoding element hHS-8 coordinately controls TNF and LTA gene expression in human T cells.

147 Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pat

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

149 These findings were driven by CSF TNF, which correlated with RM (r = 0.236, p = 0.045), an

150 antibodies against the inflammatory cytokine TNF-alpha.

151 The cytokine TNF produced by activated CD4(+) T cells engaged its rec

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

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

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

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

156 ckade of granzyme B was observed to decrease TNF production.

157 cells were hypersensitive to RIPK3-dependent TNF-induced apoptosis and necroptosis.

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

159 s suggest that endothelial R-Ras facilitates TNF-dependent transendothelial migration (diapedesis) of

160 (in particular, anti-tumour necrosis factor (TNF) agents).

161 ponse to the cytokine tumor necrosis factor (TNF) and other inflammatory stimuli.

162 , a dual inhibitor of tumor necrosis factor (TNF) and RANKL trimerization, we identified four compoun

163 nadequate response to tumor necrosis factor (TNF) inhibitors.

164 Excessive tumor necrosis factor (TNF) is known to cause significant pathology.

165 lular feedback in the tumor necrosis factor (TNF) response.

166 We demonstrate that tumor necrosis factor (TNF) signaling limits M2 granuloma macrophage polarizati

167 ut did play a role in tumor necrosis factor (TNF) signaling.

168 he early 2000s, anti-tumour necrosis factor (TNF) treatment has significantly improved treatment outc

169 ), IL-6, IL-12 (p70), tumor necrosis factor (TNF), and IL-10, was observed in mice after S. suis type

170 expression of CXCL8, tumor necrosis factor (TNF), and other proinflammatory genes.

171 rleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-alpha and IL-1beta in hospitalized patients with co

172 Administration of tumor necrosis factor (TNF)-alpha, an established HIV latency reversal agent, s

173 struction and produce tumor necrosis factor (TNF)-alpha, post-effector cells acquire innate signature

174 Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8 or TIPE) acts as a

175 erferon response and tumour necrosis factor (TNF)-induced cytotoxicity are dominant sub-phenotypes.

176 Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces a

177 o-inflammatory marker tumor necrosis-factor (TNF)-alpha.

178 idative stress [OSI], tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, matrix metalloprotei

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

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

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

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

183 cy (IL-10(+); GM-CSF(+)) and high-frequency (TNF(+)) cytokine-defined B cells.

184 d mitogen-induced upregulation of IFN-gamma, TNF, IL-6, CXCL9, CXCL10, and IL-1beta production.

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

186 The human TNF/LT locus genes TNF, LTA, and LTB are expressed in a cell type-specific

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

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

189 >=1000 copies/mL was associated with higher TNF-alpha levels (P = .013).

190 ed that CrmD is critically dependent on host TNF for its function.

191 It remains incompletely understood how TNF can lead to different disease phenotypes such as des

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

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

194 The human TNF/LT locus genes TNF, LTA, and LTB are expressed in a

195 y network mediated by RBP-J/NFATc1-miR182 in TNF-induced osteoclastogenesis and inflammatory bone res

196 atory cytokine production in lungs including TNF, IL-6, IL-10, and IFN-gamma.

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

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

199 -member 18 (TNFRSF18, glucocorticoid-induced TNF-receptor-related) and EBV-induced-3 (EBI3, an IL-35

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

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

202 increase splenic nerve activity and inhibit TNF production.

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

204 servers as a critical mechanism that limits TNF-induced osteoclast differentiation and inflammatory

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

206 23 effectively reduces neutrophil migration, TNF-alpha secretion, and tissue inflammation in mice (fe

207 TNF in combination, but neither IL-1beta nor TNF alone.

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

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

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

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

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

213 an successfully be used for the detection of TNF cleavage in flow cytometry and live-cell imaging app

214 Nonlesional AD skin exhibited enrichment of TNF, T(H)1, T(H)2, and T(H)17 response genes.

215 y and its inflammation by gene expression of TNF (tumor necrosis factor)-alpha.

216 3 [0.2-4.5]) and a higher gene expression of TNF-alpha and IL-10 at 45I-120R.

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

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

219 Expression of TNF-receptor-superfamily-member 18 (TNFRSF18, glucocorti

220 ease sensitivity and coordinate induction of TNF, LTA, and hHS-8 enhancer RNA transcription occurs.

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

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

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

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

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

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

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

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

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

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

231 sed knockout mice to investigate the role of TNF receptors 1 and 2 (TNFR1 and TNFR2), CD44, or alpha2

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

233 The use of TNF-deficient mice and those that express only membrane-

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

235 y macrophages showing IL (interleukin) 1B or TNF (tumor necrosis factor) expression as well as a foam

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

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

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

239 Clustering of patients based on plasma TNF and KYN/TRP yielded subgroups of high (N = 17) and l

240 terminus of the transmembrane portion of pro-TNF on cleavage.

241 neutralization of IL-6 or TGF-beta protected TNF(-/-) mice from an otherwise lethal infection.

242 motility, RHAMM, and the HA-binding protein TNF-stimulated gene 6 protein (TSG6).

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

244 dependent on tumor necrosis factor receptor (TNF-R) signaling.

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

246 3cr1creER Tak1fl/fl mice resulted in reduced TNF production and microglial MHC-II and improved neuroc

247 937 or THP-1 cells, the mNLS variant reduced TNF-alpha or IFN-beta mRNA expression to a similar exten

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

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

250 s function of PACRG in positively regulating TNF signaling may help to explain the association of PAC

251 etained high levels of ST6Gal-I and resisted TNF-induced apoptosis, supporting prolonged survival.

252 heat-stressed germ cells (NFkappaB response, TNF and TGFbeta signaling, Hif1alpha and Myc genes).

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

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

255 ss only membrane-associated but not secreted TNF revealed that CrmD is critically dependent on host T

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

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

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

259 expression negatively correlates with sputum TNF-alpha concentrations.

260 have DNA hypermethylation of the IL-2/STAT5, TNF/NF-kappaB, and IFN-gamma signaling pathways.

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

262 F as a genetically encoded reporter to study TNF shedding at the single-cell level.

263 -40), or inflammation (such as MCP-1, suPAR, TNF receptor-1 [TNFR-1], and TNFR-2) may identify childr

264 not increased by adding either supplemental TNF ligand or a cross-linking reagent, suggesting that t

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

266 Here, we generated C-tag TNF as a genetically encoded reporter to study TNF shedd

267 As such, C-tag TNF can successfully be used for the detection of TNF cl

268 The functionality of the C-tag TNF reporter is based on the exposure of a cryptic epito

269 for microglia in CNS-GVHD, identify the TAK1/TNF/MHC-II axis as a mediator of CNS-GVHD, and provide a

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

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

272 Collectively, these data indicate that TNF can drive distinct inflammatory pathologies.

273 In this study, we show that TNF is sufficient to upregulate MINCLE, MCL, and DECTIN-

274 eractions with other cofactors, showing that TNF has strikingly different effects depending on co-sti

275 regulator of immune evasion and suggest that TNF could be used to enhance sensitivity of tumors to im

276 The TNF receptor superfamily member OX40 (CD134) is a cell s

277 The TNF-related apoptosis-inducing ligand (TRAIL) triggers a

278 primary human CD4(+) T cells, hHS-8 and the TNF and LTA promoters display increased H3K27 acetylatio

279 Loss of ADAM17, TNF and the TNF receptor Grindelwald in pigmented glial cells of the

280 ganized during vertebrate evolution, and the TNF superfamily of genes has been identified as essentia

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

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

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

284 rway inflammation that neutralization of the TNF family cytokine TL1A through Ab blocking or genetic

285 4-1BBL, a member of the TNF superfamily, regulates the sustained production of i

286 2 results in their rapid elimination via the TNF/Eiger>JNK signalling pathway, local over-expression

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

288 aberrant signaling when the trimer binds to TNF receptor 1 (TNFR1).

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

290 kappaB (NF-kappaB) activation in response to TNF.

291 ose engineered to express only transmembrane TNF (mTNF), fully recovered.

292 ssed markedly reduced ST6Gal-I and underwent TNF-induced, caspase-mediated apoptosis, consistent with

293 Upon TNF stimulation, PACRG was recruited to the activated TN

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

295 The combined test using TNF transcript and histological score at debut of UC can

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

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

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

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

300 Treatment with TNF inhibitors in RA patients reverses the expression ch