ライフサイエンスコーパス: tumor necrosis factor

1 es by monocytes, including interleukin-6 and tumor necrosis factor.

2 ytokines (IL [interleukin] 1B, IL6, and TNF [tumor necrosis factor]).

3 mg/day, thiopurines, methotrexate); (2) anti-tumor necrosis factor agents; (3) combination therapy; a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 1-RIPK3-MLKL signaling cascade downstream of tumor necrosis factor alpha (TNF-alpha), has been implic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 0 g pellet contained a significant amount of tumor necrosis factor alpha (TNFalpha).

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

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

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

58 2 was related to biomarkers of inflammation (tumor necrosis factor alpha [P = .007]), monocyte/macrop

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

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

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

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

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

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

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

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

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

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

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

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

71 1 and induced Toll-like receptor 4-dependent tumor necrosis factor alpha production by macrophages.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 1 beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the gingival

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 -6, -8, and -10 retained the association but tumor necrosis factor-alpha, C-reactive protein, and S-1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 We examined the outcome of anti-tumor necrosis factor and anti-interleukin-12/interleuki

187 tivated protein kinase activation to control tumor necrosis factor and IL-1alpha/beta expression, and

188 nvariant NKT and CD4(+) T cells that express tumor necrosis factor and interferon gamma.

189 ells and MyD88, was exquisitely sensitive to tumor necrosis factor and interleukin-17A, and persisted

190 fications in key regulatory genes, including tumor necrosis factor and interleukin-1beta.

191 -DG and glucose starvation strongly suppress tumor necrosis factor and interleukin-6 production and c

192 r proinflammatory (interleukin [IL] 1, IL-6, tumor necrosis factor) and regulatory (IL-10) cytokine c

193 onse or intolerance to immunosuppressants or tumor necrosis factor antagonists.

194 Anti-tumor necrosis factor (anti-TNF) therapies are the most

195 Anti-tumor necrosis factor (anti-TNF) therapy resistance is a

196 kines, brain-derived neurotrophic factor and tumor necrosis factor beta, were most predictive.

197 estrogen, metformin, statins, vitamin D, and tumor necrosis factor blockers are unintentionally modul

198 ble form of the mannose receptor (CD206) and tumor necrosis factor by enzyme-linked immunosorbent ass

199 rophages showing IL (interleukin) 1B or TNF (tumor necrosis factor) expression as well as a foam cell

200 sis, indicated by the expression of the TNF (tumor necrosis factor)-family members; (2) extracellular

201 bolic syndrome (MS), inflammatory cytokines (tumor necrosis factor, high sensitive C-reactive protein

202 ling/proinflammatory pathways (drivers: TNF [tumor necrosis factor], IL-6, TREM1 [triggering receptor

203 List prices of tumor necrosis factor inhibitors (n = 3) increased by 16

204 rming growth factor beta2) and inflammation (tumor necrosis factor, interleukin 1beta).

205 omarkers (interferon-gamma, myeloperoxidase, tumor necrosis factor, interleukin 6, soluble CD14).

206 t BD(L) expression of glucocorticoid-induced tumor necrosis factor ligand (GITRL) was essential for i

207 cell contents; increased immunostaining for tumor necrosis factor ligand superfamily member 14; spar

208 Unlike all human or mouse tumor necrosis factor ligands that form noncovalent and

209 Tumor necrosis factor-like cytokine 1A (TL1A, TNFSF15) i

210 proatherogenic (such as IL-1, IL-6, and TNF [tumor necrosis factor]) or as anti-inflammatory and anti

211 tivated by NOD1 or TLR4 agonists, except for tumor necrosis factor production by MDM, which is inhibi

212 kinase-dependent Ripk1-independent IL-1 and tumor necrosis factor production, and were prone to cell

213 ytotoxic T-lymphocyte-associated protein 4), tumor necrosis factor-R-II, and CD16.

214 s in necroptosis, which is also dependent on tumor necrosis factor receptor (TNF-R) signaling.

215 A costimulatory signal from the tumor necrosis factor receptor (TNFR) family molecule OX

216 Both orthopoxviruses encode tumor necrosis factor receptor (TNFR) homologs or viral

217 ons of necroptosis related signals including tumor necrosis factor receptor (TNFR1), receptor interac

218 Ligand-induced tumor necrosis factor receptor 1 (TNFR1) activation cont

219 +14, and +21 post-HCT: stimulation-2 (ST2), tumor necrosis factor receptor 1 (TNFR1), regenerating i

220 Tumor necrosis factor receptor 1 is increased in cystic

221 beta, IL-6, IL-8, IL-10, and sTNFR1 (soluble tumor necrosis factor receptor 1) were assessed in plasm

222 TNFR1 (tumor necrosis factor receptor 1), UPAR (urokinase plasm

223 EIP-1 scores-described by soluble tumor necrosis factor receptor 2 (sTNF-R2), soluble inte

224 Tumor necrosis factor receptor 2 (TNFR2) is strongly upr

225 nse to self-antigens, and are switched on by tumor necrosis factor receptor 2 (TNFR2).

226 The tumor necrosis factor receptor 2 positive (TNFR2pos) Tre

227 , intercellular adhesion molecule-1, soluble tumor necrosis factor receptor 2, and soluble cluster of

228 nfection and that inactivation of Tregs with tumor necrosis factor receptor II (TNFR2) antagonistic a

229 Extracellular trafficking of tumor necrosis factor receptor superfamily (TNFRSF) is t

230 We report here that tumor necrosis factor receptor superfamily death recepto

231 4-1BB is a member of the tumor necrosis factor receptor superfamily, which has be

232 all integrity of LSC function, including the tumor necrosis factor receptor Tnfrsf2, whose upregulati

233 eukin-8, chitinase-3-like protein-1, soluble tumor necrosis factor receptor-1, procalcitonin [PCT], C

234 In functional and mechanistic analyses, tumor necrosis factor receptor-associated factor (TRAF)-

235 acrophage colony-stimulating factor, soluble tumor necrosis factor receptor-I, IL-1alpha, and matrix

236 tumor necrosis factor-alpha, sTNFRI [soluble tumor necrosis factor-receptor I], and interleukin-6), Y

237 reactive protein, IL6, d-dimer, and systemic tumor necrosis factor receptors I and II (P <= .05).

238 The tumor necrosis factor-related apoptosis-inducing ligand

239 r2(-/-) ) double knockout (DKO) mice lacking tumor necrosis factor-related apoptosis-inducing ligand

240 nus of conatumumab, an antibody that targets tumor necrosis factor-related apoptosis-inducing ligand

241 owed presymptomatic activation of IL-17- and tumor necrosis factor-related pathways.

242 and in patients subsequently requiring anti-tumor necrosis factor rescue therapy.

243 ns, induce type I IFN (interferon), and TNF (tumor necrosis factor) responses in endothelial cells.

244 receptor and was promoted by cell-intrinsic tumor necrosis factor signaling.

245 Tumor necrosis factor superfamily (TNFSF) members, inclu

246 of mRNAs encoding cytokines (LTB; CD40; and tumor necrosis factor superfamily [TNFSF] members TNFSF1

247 We investigate the effects of tumor necrosis factor superfamily member 14 (TNFSF14, al

248 NIK), a signaling molecule downstream of the tumor necrosis factor superfamily receptors such as CD27

249 le to tolerance induction, and released more tumor necrosis factor than SPMs.

250 phtheria toxin receptor transgenic mice, and tumor necrosis factor (TNF) alpha receptor-1 (TNFR1)(-)(

251 Tumor necrosis factor (TNF) and interferon regulatory fa

252 n and injury by inhibiting the production of tumor necrosis factor (TNF) and other cytokines in the s

253 s survive or die in response to the cytokine tumor necrosis factor (TNF) and other inflammatory stimu

254 39 analogues of SPD-304, a dual inhibitor of tumor necrosis factor (TNF) and RANKL trimerization, we

255 Addition of a microglial tumor necrosis factor (TNF) deficiency rescued these ani

256 The role of tumor necrosis factor (TNF) in the fetal intestine is po

257 tic arthritis have an inadequate response to tumor necrosis factor (TNF) inhibitors.

258 Excessive tumor necrosis factor (TNF) is known to cause significan

259 apacity, resulting in, for example, enhanced tumor necrosis factor (TNF) neutralization by two anti-T

260 in the 2 years before initiation of an anti-tumor necrosis factor (TNF) or immunomodulator therapy,

261 In vitro, tumor necrosis factor (TNF) or lymphotoxin-beta receptor

262 tability of AVX-470, a bovine colostral anti-tumor necrosis factor (TNF) polyclonal antibody used in

263 al LPS-induced intercellular feedback in the tumor necrosis factor (TNF) response.

264 We demonstrate that tumor necrosis factor (TNF) signaling limits M2 granulom

265 -deficient cells to IFNgamma was mediated by tumor necrosis factor (TNF) signaling via receptor inter

266 y a role in mitophagy but did play a role in tumor necrosis factor (TNF) signaling.

267 Conversely, anti-Tumor Necrosis Factor (TNF) therapies improve depression

268 ly reduced after remission induction by anti-tumor necrosis factor (TNF) therapy.

269 Among immune markers, plasma tumor necrosis factor (TNF) was robustly associated with

270 thelial venules by the inflammatory cytokine tumor necrosis factor (TNF) within 24 hours of pathogen

271 n of interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor (TNF), and Abeta peptides enhance

272 ing interleukin 2 (IL-2), IL-6, IL-12 (p70), tumor necrosis factor (TNF), and IL-10, was observed in

273 o called CXCL8) and the expression of CXCL8, tumor necrosis factor (TNF), and other proinflammatory g

274 nt evidence that a proinflammatory cytokine, tumor necrosis factor (TNF), can have both proangiogenic

275 at NK cells expressed more interferon-gamma, tumor necrosis factor (TNF), granzyme B, and perforin th

276 contrary, pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6 and IL-8

277 Kupffer cell loss induced tumor necrosis factor (TNF)- and interleukin-1 (IL-1) re

278 y to measure serum interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-alpha and IL-1beta in hospit

279 nor PgPE-treated PDLSCs supernatants altered tumor necrosis factor (TNF)-alpha and IL-1beta secretion

280 serum levels of LRG, interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in patients with Stage

281 tudy, we show that Msg significantly impairs tumor necrosis factor (TNF)-alpha secretion by macrophag

282 A (KDM7A) and 6A (UTX) play crucial roles in tumor necrosis factor (TNF)-alpha signaling in endotheli

283 Administration of tumor necrosis factor (TNF)-alpha, an established HIV la

284 ases in liver mRNA and protein expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1bet

285 s can trigger tissue destruction and produce tumor necrosis factor (TNF)-alpha, post-effector cells a

286 Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNF

287 by circumventing immune defenses mediated by tumor necrosis factor (TNF)-family cytokines.

288 ficient thymocytes were acutely sensitive to tumor necrosis factor (TNF)-induced cell death, Rel-defi

289 Cytokine tumor necrosis factor (TNF)-mediated macrophage polariza

290 Tumor necrosis factor (TNF)-related apoptosis-inducing l

291 -2 were exposed to interleukin (IL)1beta and tumor necrosis factor (TNF)alpha with and without UDCA.

292 esponse by HIV-infected MG-hBORGs, releasing tumor necrosis factor (TNF-alpha) and interleukin-1 (IL-

293 renal vein levels of pro-inflammatory marker tumor necrosis-factor (TNF)-alpha.

294 inflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF] and IL-1beta) and their solu

295 actor, interleukin [IL]17A, IL17F, IL22, and tumor necrosis factor [TNF]).

296 biomarkers (CXCL10, IL-1beta, IL-10, sCD14, tumor necrosis factor [TNF]-alpha, and TNF-beta) achieve

297 [MDA], glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]-alpha, interleukin [IL]-1bet

298 It provides a limit of detection for Tumor Necrosis Factor (TNFalpha) of 0.15 +/- 0.05 ng/mL

299 cell death, necroptosis can be triggered by tumor necrosis factor via the kinases RIPK1/RIPK3 and th

300 Tumor necrosis factor was both necessary and sufficient