ライフサイエンスコーパス: IL-6

1 IL-6 also stabilizes Snail1 by inducing Dub3 expression,

2 IL-6 and osteopontin correlated significantly with radio

3 IL-6 is a pleiotropic cytokine with a wide range of biol

4 IL-6 is a pleiotropic proinflammatory cytokine that is e

5 IL-6 may crucially regulate this process; however, the u

6 IL-6 production by macrophages is dramatically increased

7 IL-6 signaling was increased by Gab2 overexpression and

8 IL-6 signals are transmitted via the transmembrane glyco

9 IL-6 trans-signaling, and not IL-6 classic signaling, is

10 IL-6 upregulates Mcl-1 transcription in a STAT3-dependen

11 IL-6 was upregulated only 1 day after the procedure, but

12 IL-6/IL-6R signaling pathway, in particular, has been pr

13 pression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

14 ssion of monocyte chemoattractant protein-1, IL-6, IL-1beta, and insulin-like growth factor-1.

15 SCs with monocyte chemoattractant protein-1, IL-6, IL-1beta, and is associated with increased MyoD ex

16 es and adhesion molecules, including VCAM-1, IL-6, ICAM-1, E-selectin, and monocyte chemoattractant p

17 quired for induction of interleukin (IL)-10, IL-6, and IL-1beta cytokines.

18 Expression of IL-17A, IL-6 and IL-8 and neutrophil numbers was significantly e

19 BAL fluid myeloperoxidase, IL-8, IL-1alpha, IL-6, granulocyte colony-stimulating factor, and GM-CSF

20 ic asthma and increased BAL fluid IL-1alpha, IL-6, IL-8, granulocyte colony-stimulating factor, and G

21 sms in the genes for interleukin (IL)-1beta, IL-6, IL-10, monocyte chemoattractant protein-1, tumor n

22 atory genes (TNF-alpha, IFN-gamma, IL-1beta, IL-6, and CCL2 mRNAs), and attenuated the wasting syndro

23 pressed lower levels of TNF-alpha, IL-1beta, IL-6, and IL-10 compared with cells from WT mice, but bo

24 of the TH17-instructing cytokines IL-1beta, IL-6, and IL-23, whereas HDM-specific TH2 cell different

25 tory cytokines, such as TNF-alpha, IL-1beta, IL-6, and IL-23.

26 L-1beta, IL-6, and IL-8, increased IL-1beta, IL-6, and IL-8 in fetal lung, intestine, and brain, and

27 R-transrepressed promoters such as IL-1beta, IL-6, and IL-8 Taken together, our data establish ACTN4

28 in WBCs, elevated plasma levels of IL-1beta, IL-6, and IL-8, increased IL-1beta, IL-6, and IL-8 in fe

29 ntly stimulate cytokine TNF-alpha, IL-1beta, IL-6, IL-10, and IL-12 production in human monocytes.

30 typical of inflammatory responses (IL-1beta, IL-6, IL-10, TNF).

31 y (CD68, CD206, FOXP3), cytokines (IL-1beta, IL-6, IL-10, TNF-alpha) and oxidative stress (superoxide

32 7-predominant asthma had increased IL-1beta, IL-6, IL-23, C3a, and serum amyloid A levels in BAL flui

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

34 ntrations of angiopoietin-1, angiopoietin-2, IL-6, IL-8, soluble tumor necrosis factor receptor-1, so

35 nstrated either high (IL-8, IFN-gamma, IL-2, IL-6, and IL-1beta) or low (IL-15, TNF-alpha, IL-12 p70,

36 centrations of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor necros

37 SD1 deficiency though plasma levels of IL-4, IL-6 and TNF-alpha were slightly affected by 11beta-HSD1

38 ntification of interleukin (IL)-1beta, IL-4, IL-6, IL-17, and tumor necrosis factor-alpha using an as

39 ical damage, via induction of interleukin 6 (IL-6) from epithelial cells, tailored effector T cell fu

40 mouse strain, in which human interleukin 6 (IL-6) gene encoding the cytokine that is important for B

41 The cellular sources of interleukin 6 (IL-6) that are relevant for differentiation of the TH17

42 -FABP), soluble CD14 (sCD14), interleukin 6 (IL-6), and C-reactive protein (CRP) at 6 weeks and 6 mon

43 lloproteases and synthesis of interleukin 6 (IL-6).

44 enous soluble factors such as interleukin-6 (IL-6) and APRIL, to prevent their cell death.

45 of many cytokines, including interleukin-6 (IL-6) and IL-10.

46 RP) and a panel of cytokines (interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)), were

47 for the selective capture of interleukin-6 (IL-6) as targeted antigen.

48 ication mechanism mediated by interleukin-6 (IL-6) cytokine secreted from EGFRvIII-positive tumor cel

49 suppressing pro-inflammatory interleukin-6 (IL-6) expression after interleukin-1 beta (IL-1beta) sti

50 osis factor alpha (TNF-alpha)/interleukin-6 (IL-6) in infected kidneys.

51 on of the peripheral cytokine interleukin-6 (IL-6) into brain parenchyma and subsequent expression of

52 tran gut translocation, serum interleukin-6 (IL-6) levels, bacteremia, and sepsis mortality.

53 PB interleukin-6 (IL-6) negatively correlated with endothelial colony-form

54 yte-derived cytokine (KC) and interleukin-6 (IL-6) production by cells.

55 the pro-inflammatory cytokine interleukin-6 (IL-6) relative to BALB/cJ and PDE11A WT mice, respective

56 Interleukin-6 (IL-6) was identified as a regulator of mIndy by binding

57 The inflammatory cytokine, interleukin-6 (IL-6), is a critical mediator of HCC development.

58 mor necrosis factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitment, and a lower bacteria

59 omass, systemic inflammation (interleukin 6 [IL-6]), endothelial activation (angiopoietin-2), and mic

60 cellular adhesion molecule 1; interleukin 6 [IL-6]; stromal cell-derived factor 1; tissue inhibitor o

61 lungs, consistent with expression of ESAT-6, IL-6 and phosphorylated-STAT3 in Mtb-infected mouse lung

62 Blocking neither IL-6Ralpha/IL-6 nor IL-10 affected ESAT-6-induced STAT3 activation

63 reased neutrophils and serum levels of IL-8, IL-6, and MCP-1 which varied with cause of death.

64 In addition, IL-6, via STAT3-mediated feedback to mitochondria, auton

65 In addition, IL-6-type cytokines may increase the release of leptin f

66 duced inflammation (MCP-1, MIP-2, TNF-alpha, IL-6 and CD68), decreased accumulation of bone marrow-de

67 and the proinflammatory cytokines TNF-alpha, IL-6, and IL-12.

68 ses (lower IL-10 and CCL2, higher TNF-alpha, IL-6, and IL-1beta) toward pathogenic stimuli, a process

69 f IL-12 and IFN-gamma, but not of TNF-alpha, IL-6, and IL-8 upon subsequent infection with Burkholder

70 pro-B-type natriuretic peptide), TNF-alpha, IL-6, IL-12, IL-17, malondialdehyde, and fetuin-a.

71 lammatory cytokines in the serum (TNF-alpha, IL-6, IL-12, TGF-beta, and VEGF) were down regulated by

72 splicing of IL-32gamma to IL-32beta and also IL-6, IL-8, and CXCR1 signaling pathways to reverse the

73 Although IL-6 promoted virus-specific T cell responses, uncontrol

74 While ambient IL-6 was sufficient to suppress the induction of express

75 is study did not reveal any evidence that an IL-6 receptor antibody affects behavioral outcomes in sc

76 purpose of this trial was to test whether an IL-6 receptor antibody, tocilizumab, would improve resid

77 To analyze IL-6 effects in the repair phase, compounds were injecte

78 lassic signaling using the membrane-anchored IL-6 receptor and trans-signaling using its soluble form

79 MPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated.

80 ntiation was hampered by increased IL-12 and IL-6 production.

81 amoeba produced significantly less IL-12 and IL-6 than the Neff strain.

82 ant production of interleukin-12 (IL-12) and IL-6.

83 with a predominant secretion of IL-1beta and IL-6, a result confirmed in human term placental explant

84 tor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 in the synovial membrane.

85 release of some cytokines, such as IL-2 and IL-6.

86 affected ESAT-6-induced STAT3 activation and IL-6 production.

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

88 ce that MenA inhibitors act as TNF-alpha and IL-6 inhibitors, raising the potential for development a

89 and 7c and found decreases in TNF-alpha and IL-6 release and increase in IL-1beta.

90 tumor necrosis factor alpha (TNF-alpha), and IL-6.

91 attractant protein 1 (MCP-1), TNF-alpha, and IL-6 and hepatic cleaved caspase 3 in mice fed either a

92 ificant increase in IL-1beta, TNF-alpha, and IL-6 messenger RNA (mRNA) expression and positive staini

93 ry cytokines, including iNOS, TNF-alpha, and IL-6.

94 tumor necrosis factor-alpha [TNF-alpha], and IL-6) by quantitative reverse transcription polymerase c

95 To investigate the role of TGF-beta and IL-6 in myofibroblasts (MFs) - lung cancer cell interact

96 Our study demontrated that the TGF-beta and IL-6/JAK2/STAT3 signaling pathways form a positive feedb

97 significant decreases in F2-isoprostane and IL-6 concentrations.

98 yrin IX more efficiently attenuated PGE2 and IL-6 release in HG+IL-1beta-treated cells than in NG+IL-

99 not CFP10 induced STAT3 phosphorylation and IL-6 expression in the mouse lungs, consistent with expr

100 ers (high-sensitivity C-reactive protein and IL-6) and activated monocytes (CD14dimCD16+; nonclassica

101 7], Flt3L, stem cell factor [SCF], ThPO, and IL-6) from bone marrow mesenchymal stromal cells (MSCs)

102 The specific anti IL-6 antibody was immobilized and a quantitative analysi

103 uring the inflammatory phase, either an anti-IL-6 antibody, which inhibits IL-6 classic and trans-sig

104 n of Il6, treatment with a neutralizing anti-IL-6 antibody or administration of a small-molecule JAK

105 ent of wild-type mice with neutralizing anti-IL-6 mAb.

106 This suggests that anti-IL-6/IL-6R blockade could be effective in modifying T- a

107 Among these is tocilizumab (anti-IL-6 receptor [IL-6R]) which holds promise for modulatin

108 pha downward arrow, IL-1beta downward arrow, IL-6 downward arrow, HMGB1 downward arrow, MPO downward

109 l balance of inflammatory cytokines, such as IL-6 and IL-8, in primary human periodontal fibroblasts.

110 ng pNFkappaB transcriptional targets such as IL-6, IL-8, and the apoptosis inhibitor cIAP2.

111 ypic NF-kappaB family member) was reduced at IL-6 and CCL5 promoters.

112 This work demonstrates that autocrine IL-6 signaling in the gut epithelium regulates crypt hom

113 nt molecular brake that blocks the autocrine IL-6- and IL-21-induced Th17 differentiation pathways in

114 Besides IL-6, this autorine loop also drove the production of ot

115 le of IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL-6/MMP-9 immunoexpression was evaluated

116 In addition, rapid clearance of the BiSAb.IL-6 complex was observed in mice while the parental ant

117 Blocking IL-6 or downstream signaling restored Bcl-2/Bcl-xL depen

118 The stimulation of autophagy by IL-6 is regulated via multiple complementary mechanisms

119 ether VEGF release by HPMCs is controlled by IL-6 in combination with its soluble receptor (IL-6 tran

120 This aberrant LGR4 expression is driven by IL-6/STAT3 signaling and allows MM cells to hijack R-spo

121 s and CTM-167 cell lines) were stimulated by IL-6, MF-conditioned medium (MF-CM) or MFs, with or with

122 altered by NF-kappaB in response to TNF, by IL-6 via STAT3, and in response to IFN-gamma.

123 h differential, D-dimer, fibrinogen, C3, C4, IL-6, etc.

124 tion of IL-6 by DC-bound IL-6Ralpha (called 'IL-6 cluster signaling' here) was needed to prevent prem

125 osis factor alpha (TNF-alpha), CXCL10, CCL5, IL-6, and superoxide dismutase, in human macrophages inf

126 In obese humans, B cell IL-6 secretion was lowered and IgM levels were elevated

127 f pro-inflammatory cytokines and chemokines (IL-6, IFN-gamma, TNF-alpha, CXCL1, and CCL2) and extensi

128 Circulating IL-6 is thought to maintain energy status during exercis

129 e CD163 (sCD163), soluble CD14 (sCD14), CRP, IL-6, and a gut microbial translocation marker (intestin

130 ter amounts of the pro-inflammatory cytokine IL-6, compared to those from normal-weight patients (p <

131 paB pathway and the proinflammatory cytokine IL-6 in autoantibody production, but not IFN regulatory

132 t 6 h we detect the proinflammatory cytokine IL-6 in the hippocampus, followed up by alterations in t

133 Notably, cytokines IL-6, TNF, and IFN-gamma and chemokines CCL2, CCL3, and

134 production of the proinflammatory cytokines IL-6 and IL-12p40 while enhancing the release of the reg

135 tinocytes, and type I IFN blockade decreased IL-6 secretion by lupus keratinocytes.

136 We also see evidence of decreased IL-6 pathway signaling in islets from donors with type 2

137 Myoferlin knockdown significantly decreased IL-6-mediated tumor cell migration, tumorsphere formatio

138 n preclinical models suggest that decreasing IL-6 activity may mitigate or reverse some of these defi

139 ndritic cells, potentiates the p65-dependent IL-6 and the p38-MK2/3-dependent IL-13 production.

140 broblasts was induced by chondrocyte-derived IL-6.

141 Although treatment with either IL-6 or soluble IL-6 receptor (sIL-6R) alone had no effe

142 In response to prolonged exercise, IL-6 is synthesized by contracting skeletal muscle and r

143 this study first demonstrated that exogenous IL-6 promoted crypt organoid proliferation and increased

144 In vitro exogenous IL-6-induced IL-17 production in iTreg cells, and in viv

145 and that the crypt epithelium also expressed IL-6.

146 y which SMYD2 might be induced by cyst fluid IL-6 and TNF-alpha in ADPKD kidneys.

147 smokers (OR = 1.99, 95% CI: 1.15, 3.44) for IL-6 and among former smokers (OR = 2.83, 95% CI: 1.18,

148 lation of autophagy as a novel mechanism for IL-6-mediated protection of beta cells from stress-induc

149 Thus, lupus keratinocytes are primed for IL-6 hyperproduction in a type I IFN-dependent manner.

150 lencing revealed that STAT4 was required for IL-6 transcription.

151 (mRNA) expression and positive staining for IL-6.

152 els of many pro-inflammatory cytokines (e.g. IL-6, MCP-1, IL-22, TNF-alpha) and pronounced complement

153 Neutralization of IL-10 increased IFN-gamma, IL-6 and TNF-alpha production and improved bacteria kill

154 y cytokines, including TNF-alpha, IFN-gamma, IL-6, and CCL2.

155 the transcription of proinflammatory genes (IL-6, CCL-2, and CCL-5).

156 Global IL-6 inhibition during the repair phase disturbed bone f

157 Global IL-6 inhibition in the early phase after fracture reduce

158 Histamine, IL-6, IL-17, IL-21 and IL-22 induced the expression of H

159 The provision of human IL-6 not only enhanced thymopoiesis and periphery T-cell

160 We conclude that human IL-6 knock-in mice represent a novel and improved model

161 Neutralization studies identified IL-6 and CXCL8 as factors secreted by EVTs that induce e

162 nflammatory factors such as IgG1, IgG2, IgM, IL-6 and PMPhi phagocytosis, stimulation of secretion of

163 important for innate and acquired immunity, IL-6 trans-signaling has been linked to accelerated live

164 The primary outcome was change in IL-6 level from day 1 to 14.

165 In nonresponders, the percent change in IL-6 on the day after TAE (P = .033) and the mean percen

166 Furthermore, changes in IL-6 following stress predicted intraindividual variabil

167 , whereas it led to significant decreases in IL-6 and Podoplanin expression.

168 However, sustained elevations in IL-6 due to repeated bouts of unaccustomed activities or

169 alveolar type 2 progenitor cells, including IL-6/Stat3, Bmp, and Fgf signaling.

170 infiltrate and secrete cytokines, including IL-6, to repair skeletal muscle damage.

171 e suppression of catabolic markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in

172 ed in acute pancreatitis patients, including IL-6, tumor necrosis factor-alpha, IL-1beta, chemokine (

173 P-deficient monocytes demonstrated increased IL-6, increased nitrite, and decreased bacterial replica

174 , IL-17A and aeroallergens further increased IL-6 and IL-8 production synergistically.

175 erferons (IFN-alpha and IFN-kappa) increased IL-6 production by control keratinocytes, and type I IFN

176 HDL that increased IL-6 secretion were enriched in ApoC-III, di-sialylated

177 ith increased BM function, whereas increased IL-6 was associated with BM impairment.

178 mechanism whereby RB inactivation increases IL-6 production in MCF-7 cells appeared to involve fatty

179 All of the studied NPs did not induce IL-6 release by the lung and immune cells.

180 AT1R knockdown impaired IL-1beta-induced IL-6 and IL-8 secretion in cultured HGF and HPLF.

181 Aa-induced IL-6 and IL-8 production was inhibited by rosuvastatin,

182 c small interfering RNA enhanced LPS-induced IL-6 and TNF-alpha expression.

183 pha and COX-2, while PPH reduced LPS-induced IL-6 and TNF-alpha responses.

184 ESAT-6 but not Pam3CSK4 induced IL-6 by TLR2 knockout BMDM.

185 either an anti-IL-6 antibody, which inhibits IL-6 classic and trans-signaling, or soluble glycoprotei

186 able to block the induction of interleukins IL-6 and IL-8 triggered by pathologic stimuli relevant t

187 PS challenge, serum levels of TNF-alpha, KC, IL-6, and IL-10 were significantly increased in lyM-PP2A

188 le gp130 fused to Fc transgenic mice lacking IL-6 trans-signaling are largely protected from tumor fo

189 Maternal HFD also increased plasma leptin, IL-6, and MCP-1 in WT and increased arcuate expression o

190 findings identify a novel mechanism linking IL-6 trans-signaling and angiogenesis in the peritoneal

191 Elevated mRNA expression of liver IL-6, IL-17A, IL-17F, TGF-beta1, alpha-SMA, TGR5, NTCP,

192 e found that proinflammatory stimulants LPS, IL-6 and IL-1beta up-regulated the expression of HCA2 on

193 did not affect ESAT-6 stimulated macrophage IL-6 production.

194 e conclude that ESAT-6 stimulates macrophage IL-6 production through STAT3 activation.

195 IL-6 trans-signaling, and not IL-6 classic signaling, is mandatory for development of

196 icant reductions of IL-17 and IL-23, but not IL-6 and TNF-alpha, whereas IL-10 levels were increased

197 , we show that IL-6 trans-signaling, but not IL-6 classic signaling, is essential to promote hepatoce

198 evated production of cytokines, most notably IL-6.

199 reaction, IL-6 immunostaining, activation of IL-6/signal transducer and activator of transcription (S

200 and a quantitative analysis of the amount of IL-6 captured by the immuno-affinity membrane was perfor

201 Here, we explore the biology of IL-6/IL-6R interactions and the evidence for an importan

202 -density cells treated with a combination of IL-6/8.

203 Furthermore, combinatorial detection of IL-6 and Cortisol in human sweat was established with mi

204 Limit of detection of IL-6 in human sweat was 0.2 pg/mL for 0-24 hours and 2 p

205 medium with Neu5Ac stimulated expression of IL-6 and IL-8 and rescued the tumor growth and migratory

206 helial migration via increased expression of IL-6 and monocyte chemoattractant protein 1 (MCP-1).

207 yperplasia, reduced epithelial expression of IL-6 and TNF-alpha, and impaired bacterial clearance.

208 ation of RelA with a decreased expression of IL-6, IL-12p40, and IL-17A.

209 pi-LXA4 and MaR1 and regulated expression of IL-6, PDPN and STAT-1.

210 To study the function of IL-6 during the inflammatory phase, either an anti-IL-6

211 ene of IL-6 and determine novel functions of IL-6 through mINDY.

212 our data identify mIndy as a target gene of IL-6 and determine novel functions of IL-6 through mINDY

213 Simultaneous inhibition of IL-6/8 receptors decreases the expression of WASF3 and A

214 orsened over time, suggesting that a lack of IL-6 led to compensatory proinflammatory effects by othe

215 t demonstrated significantly lower levels of IL-6 and IFN-gamma (p < 0.0001), which is likely to have

216 iC3b or fibrinogen, the expression levels of IL-6 and TNF-alpha in integrin alphaM(PS)beta2 BMDMs wer

217 0.05), which reflected the greater levels of IL-6 detected in the synovial fluid of the obese OA pati

218 pathology to its diagnosis and the levels of IL-6 secretion induced by LPS.

219 classical monocytes secreted high levels of IL-6, the blockade of which resulted in increased neutro

220 culture systems, MFs secreted high levels of IL-6, while cancer cells produced high levels of TGF-bet

221 antibodies prolonged the serum half-life of IL-6.

222 imals was associated with reduced numbers of IL-6-producing macrophages in the inflamed colonic lamin

223 ctor Foxp3 in T cells, trans-presentation of IL-6 by DC-bound IL-6Ralpha (called 'IL-6 cluster signal

224 onmental stimuli to induce the production of IL-6 and neutrophil chemotaxins.

225 into the brain and microglial production of IL-6 and TNF-alpha.

226 ine leptin, leading to greater production of IL-6 in OA patients.

227 Plasmablast production of IL-6 is critical for initiation of T follicular helper c

228 healthy controls and favoured production of IL-6 when cultured with healthy macrophages, in contrast

229 cells, resulting in increased production of IL-6, a pleiotropic cytokine that is implicated in infla

230 Thereby, p65 mediates the production of IL-6, but not of IL-13, whereas the p38-Mapk-activated p

231 4H] mutant, but the late-phase production of IL-6, IL-12, and TNFalpha (controlled only by the pseudo

232 ritic cells, IL-33 induces the production of IL-6, IL-13, and TNF-alpha.

233 (-/-) corneas also showed down-regulation of IL-6 and CXCL1 genes with and without bacterial challeng

234 howed significant epidermal up-regulation of IL-6 compared with control via real-time PCR and immunoh

235 ns and the evidence for an important role of IL-6 in mediating allograft rejection.

236 ns for future research exploring the role of IL-6 in the adaptive response to exercise.-Hennigar, S.

237 To confirm a possible modulatory role of IL-6 on MMPs, the relationship between IL-6/MMP-1 and IL

238 In contrast, IL-1beta-induced secretion of IL-6 and IL-8 was not influenced by losartan in HGF or H

239 nd PD-L1, a higher constitutive secretion of IL-6 and increased basal alphaSMA levels.

240 s and peripheral blood monocyte secretion of IL-6 and TNF-alpha.

241 ls (mainly) and eosinophils and secretion of IL-6, TNF-alpha, and IL-17 in contrast to the eosinophil

242 atory IL-10, and stimulated the secretion of IL-6.

243 ndrial respiration and downstream targets of IL-6.

244 ibility to IL-4 or IL-13 treatment depend on IL-6 signaling, which seems to be the underlying mechani

245 ulated by SOCS3 via a mechanism dependent on IL-6 and expression of sex hormones.

246 Enhanced helper responses are dependent on IL-6 production by the activated APC.

247 A and IL-22, but not IL-1alpha, IL-1beta, or IL-6, production.

248 The mean change in plasma IL-6 levels between groups was -0.79 log10 units (-2.06

249 L-6Ralpha), Sirpalpha(+) DCs trans-presented IL-6 to T cells during the process of cognate interactio

250 rse transcription polymerase chain reaction, IL-6 immunostaining, activation of IL-6/signal transduce

251 -6 in combination with its soluble receptor (IL-6 trans-signaling).

252 erred iTreg cells was dependent on recipient IL-6.

253 Recombinant IL-6 and MF-CM activated STAT3 and upregulated TGF-beta

254 sepsis or trauma, ganciclovir did not reduce IL-6 levels and the current study does not support routi

255 ies born to obese mothers generate a reduced IL-6/TNF-alpha response to TLR 1/2 and 4 ligands compare

256 uced diminished STAT3 activation and reduced IL-6 production compared to wild type and esat-6 complem

257 While CD11c+ cell depletion reduced IL-6, IL-1beta, CXCL1, CXCL2 and CXCL10 transcriptional

258 Interestingly, reduced IL-6 and IL-8 levels were observed in HCAECs stimulated

259 hypothesize that this antiulcer drug reduces IL-6, MMP-1, and MMP-9 immunoexpression in gingiva with

260 Up-regulated IL-6, IL-8, CD38, and CD69 and down-regulated macrophage

261 ths, HIV-infected infants had highest sCD14, IL-6, and CRP concentrations (P < .001) and marginally h

262 Second, IL-6 trans-signaling directly induces endothelial cell p

263 enal inflammation in cyst development: SMYD2/IL-6/STAT3/SMYD2 and SMYD2/TNF-alpha/NF-kappaB/SMYD2.

264 though treatment with either IL-6 or soluble IL-6 receptor (sIL-6R) alone had no effect on VEGF produ

265 on to GF(+) matrix resulted in the strongest IL-6 and matrix metalloproteinase-3 release, and was eve

266 tocrine LIF, LIFR, and STAT4 drove sustained IL-6 transcription.

267 We conclude that IL-6 acts as a Th2 cytokine in obesity by stimulating M2

268 the inflammatory mechanism demonstrated that IL-6 secretion from synovial fibroblasts was induced by

269 Functional studies demonstrated that IL-6-induced in vitro crypt organoid proliferation and c

270 We thus hypothesized that IL-6-type cytokine signaling in adipocytes may regulate

271 Here, we show that IL-6 trans-signaling, but not IL-6 classic signaling, is

272 utritional interventions that may affect the IL-6 response to exercise in healthy human adults and pr

273 distinct pathways: the IL-6 classic and the IL-6 trans-signaling pathway.

274 tively, these data reveal a key role for the IL-6/STAT3 axis in potentiating FGF19-driven HCC in mice

275 A total of 29 genes from the IL-6/STAT3 pathway were upregulated on PgPE stimulation.

276 aling module mediates the IL-13, but not the IL-6, production.

277 With adequate rest and nutrition, the IL-6 response to exercise is attenuated as skeletal musc

278 s STAT3 and induces the proliferation of the IL-6-dependent B9 mouse plasmacytoma cell line.

279 r, resulting in epithelial expression of the IL-6-like cytokine Upd3, leading to activation of JAK/ST

280 an signal through two distinct pathways: the IL-6 classic and the IL-6 trans-signaling pathway.

281 melid single domain antibody recognizing the IL-6-gp80 complex but not the individual components alon

282 Immunolabeling studies showed that the IL-6 receptor was restricted to the basal membrane of Pa

283 Using their IL-6 receptor alpha-chain (IL-6Ralpha), Sirpalpha(+) DCs

284 vate STAT3 signalling in hepatocytes through IL-6 produced in the liver microenvironment.

285 ines, including tumor necrosis factor (TNF), IL-6, IL-12, IL-23, and IL-1beta.

286 of cytokines/chemokines, including TNFalpha, IL-6, IL-8, CCL4, and CCL5, by human macrophages stimula

287 ed naive CD4 T cells respond suboptimally to IL-6 compared with young cells, such that higher doses a

288 irus-specific T cell responses, uncontrolled IL-6 expression in Ifitm3-/- mice triggered the loss of

289 rnesses synergistic paracrine signalling via IL-6/8, which is amplified by cell proliferation and cel

290 In vivo IL-6 infusion stimulates a robust increase in lysosomes

291 Whereas IL-6 classic signaling is important for innate and acqui

292 hibitors develop new onset psoriasis and why IL-6 blockade for the treatment of psoriasis has not bee

293 With IL-6 treatment alone, STAT3 does not efficiently bind 20

294 Risk associations with IL-6 and IL-8 were observed for blood samples taken clos

295 Conditioned medium from HPMCs cultured with IL-6 and sIL-6R promoted angiogenic endothelial tube for

296 n VEGF production, stimulation of HPMCs with IL-6 in combination with sIL-6R promoted VEGF expression

297 bioactivity was reduced by interference with IL-6 trans-signaling.

298 regions of VHH6 interact simultaneously with IL-6 and gp80, locking the two proteins together.

299 y patients with arthritis being treated with IL-6 inhibitors develop new onset psoriasis and why IL-6

300 lyses of genes coordinately upregulated with IL-6 pointed to STAT4 and leukemia inhibitory factor (LI