ライフサイエンスコーパス: IL-6

1 IL-6 and IL-10 were not affected by any of the treatment

2 IL-6 binds to the IL-6R alpha-chain (IL-6Ralpha) and sig

3 IL-6 levels were lower for TG1.

4 IL-6 overexpression promoted activation of CD4(+) T cell

5 IL-6 stimulation augmented mTOR activation in iMCD patie

6 IL-6 transcriptional dysregulation is commonly seen in p

7 IL-6, CRP and triglycerides are likely to be causally li

8 IL-6-directed therapeutics include monoclonal antibodies

9 Levels of serum IL-10 (p = 0.0001), IL-6 (p = 0.002), MIP-3alpha (p = 0.02) and CD40-L level

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

11 -inflammatory responses including high IL-10:IL-6 and kynurenine to tryptophan ratios show less sever

12 specifically responsible for T(h)17 (IL-17, IL-6, G-CSF) and T(h)1 differentiation and expression (I

13 In 1973, IL-6 was identified as a soluble factor that is secreted

14 high levels of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17, interferon-gamma and different

15 noassay, we measured interleukin (IL) 1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and high-

16 Colonic interleukin (IL)-1beta, IL-6, and malondialdehyde (MDA) levels were measured.

17 larly, there were higher levels of IL-1beta, IL-6 and IL-8 cytokines were quantified in keratitis cau

18 kines tumor necrosis factor-alpha, IL-1beta, IL-6, and IL-12p40 are produced in lung tissue after adm

19 inflammatory cytokines, including IL-1beta, IL-6, and TNF-alpha, in adulthood.

20 peak days of infection, levels of IL-1beta, IL-6, CSF3, and CXCL2 were reduced in Il1a(-/-) oviduct

21 ase in pro-inflammatory cytokines (IL-1beta, IL-6, IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-a

22 sociated with death (interleukin [IL]-1beta, IL-6).

23 nflammatory markers (interleukin [IL]-1beta, IL-6, and tumor necrosis factor-alpha) were observed in

24 on inhibition, at least through the IL-1beta/IL-6 signaling pathway, reduces the incidence of anemia

25 nificant dysregulation of IFN-gamma, IL-1RA, IL-6, IL-10, IL-19, monocyte chemoattractant protein (MC

26 lood and in the lungs, most notably, IL-1RA, IL-6, IL-8, IP-10, and monocyte chemoattactant protein-1

27 n the serum, including interleukin 2 (IL-2), IL-6, IL-12 (p70), tumor necrosis factor (TNF), and IL-1

28 ytokines (eg, interleukin-12 [IL-12], IL-23, IL-6, IL-27, IL-10, transforming growth factor-beta) tha

29 nflammatory cytokines (interleukin-4 [IL-4], IL-6, and IL-10) and MCP-1/CCL2 were detected early afte

30 ng RSV infection (i.e., CCL-2, CCL-3, CCL-5, IL-6) as well as decreased MHC class II and costimulator

31 f 0.99, 0.93, 0.99, 0.96, and 0.75 for IL-5, IL-6, IL-10, IL-22, and TNFalpha, respectively.

32 ing on levels of IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamma, GM-

33 Circulating interleukin 6 (IL-6) levels surge during exercise and IL-6 favors exerc

34 F was not regulated by either interleukin 6 (IL-6) or IL-23, which are both potent inducers of GVHD-i

35 sed hyperalgesic priming with interleukin 6 (IL-6) priming and PGE(2) as a second stimulus as a model

36 ers C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were

37 s factor alpha (TNFalpha) and interleukin 6 (IL-6), as well as Kelch-like ECH-associating protein 1 (

38 flammatory markers, including interleukin 6 (IL-6), IL-1alpha, and tumor necrosis factor alpha (TNF-a

39 ncluding the up-regulation of interleukin 6 (IL-6), IL-23, Arginase1, as well as surface expression o

40 asuring interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 22 (IL-22), a

41 n 10, soluble CD163 (sCD163), interleukin 6 (IL-6), interleukin 18, monocyte chemoattractant protein

42 hemokine induction, including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and CXCL

43 troduced for the detection of interleukin 6 (IL-6).

44 rleukin-1beta (IL-1beta), and interleukin-6 (IL-6) after chelation therapy.

45 of the inflammatory cytokine interleukin-6 (IL-6) and decreased levels of IL-12, IFN-gamma, and the

46 we establish that endogenous interleukin-6 (IL-6) can be quantified in 2-uL serum samples from chime

47 Interleukin-6 (IL-6) has emerged as a key component of the immune respo

48 Interleukin-6 (IL-6) induced hepcidin expression is a key mediator of s

49 Interleukin-6 (IL-6) is a cytokine with critical innate and adaptive im

50 Interleukin-6 (IL-6) is a pleiotropic cytokine that has been shown to b

51 The interleukin-6 (IL-6) membrane receptor and its circulating soluble form

52 factor alpha (TNF-alpha) and interleukin-6 (IL-6) mRNAs, as well as IFN-alpha, IFN-beta, and TNF-alp

53 ects, including inhibition of interleukin-6 (IL-6) that plays a key role in the development of severe

54 a are critically dependent on interleukin-6 (IL-6) trans-signaling via the soluble IL-6 receptor (IL-

55 suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are likely causal ri

56 nterleukin-1 beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in th

57 re illness); and (3) elevated interleukin-6 (IL-6), IL-8, and myeloperoxidase levels in the airway ar

58 the proinflammatory cytokine interleukin-6 (IL-6), suggesting that MSH3 may be a shuttling protein.

59 C-reactive protein (CRP) and interleukin-6 (IL-6).

60 otein 3alpha (REG3alpha), and interleukin-6 (IL-6).

61 inflammatory cytokines (e.g., interleukin-6 [IL-6] and IL-10), in mycobacterial infection.

62 aptor molecule-1 [Iba-1]) and interleukin-6 [IL-6]) and astrogliosis/astrocyte damage (glial fibrilla

63 aB target genes include the STAT3-activating IL-6 family cytokines, expression of these messenger RNA

64 h effects on mitochondrial physiology, acute IL-6 exposure induced several mitochondrial adaptations,

65 Additionally, IL-6-deficient asthmatic mice exhibited reduced goblet c

66 pares levels of tumor necrosis factor alpha, IL-6, and IL-8 in critically ill patients with coronavir

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

68 results in reduced production of TNF-alpha, IL-6, and IL-1beta and in limited M1 macrophage polariza

69 ion of proinflammatory cytokines (TNF-alpha, IL-6, and IL-1beta) that are associated with activation

70 type with decreased production of TNF-alpha, IL-6, IL-12p70, IL-10, GM-CSF, VEGF, MIP-1beta, TNF-beta

71 LR3, or TLR4 agonists, as well as TNF-alpha, IL-6, or IL-17A, but not IFN-gamma, similarly induced sH

72 s IL (interleukin)-1beta (98%, P<0.0001) and IL-6 (460%, P<0.02) compared with nonfailing hMSCs.

73 is (CTP 7-9) were IP-10 (p-value= 0.008) and IL-6 (p-value=0.002).

74 human monocyte-dependent release of IL-1 and IL-6 in a xenotransplanted B-cell lymphoma model without

75 6 predominated in WT mice, whereas MCP-1 and IL-6 predominated in IRF3-KO mice.

76 nse, such as CXCL1, CXCL6, PDGF-A, MCP-1 and IL-6.

77 evels did not change, and sCD163, MCP-1, and IL-6 levels changed at a single time point.

78 sTREM-1- and IL-6-based algorithms are highly sensitive to identify p

79 Serum IL-10 and IL-6 were significantly elevated at presentation, and IL

80 iver cirrhosis (CTP score), mainly IP-10 and IL-6, which discriminated patients with Child-Pugh B con

81 ry tumorigenic cytokines, such as IL-17A and IL-6, and increased STAT3 tyrosine phosphorylation.

82 with lower levels of interleukin (IL)-18 and IL-6 before and up to 12 weeks post-ART initiation (Benj

83 evated signatures of inflammation (IL-18 and IL-6), lymphocytic and myeloid chemotaxis and activation

84 ssential role of B cell-derived IL-1beta and IL-6 during homeostatic T cell expansion in a clinically

85 ell production of interleukin (IL)-1beta and IL-6 is markedly upregulated after heart allotransplanta

86 ncreased macrophages, increased IL-1beta and IL-6 levels, anemia and thrombocytopenia.

87 nts produced significantly more IL-1beta and IL-6, cytokines known to drive Th17 cell differentiation

88 e network differed: TNF-alpha, IL-1beta, and IL-6 predominated in WT mice, whereas MCP-1 and IL-6 pre

89 flammatory factors (TNF-alpha, IL-1beta, and IL-6) and up-regulate an anti-inflammatory factor (IL-10

90 Th1 (IL-12)- and Th17 (IL-23, IL-1beta, and IL-6)-conditioning cytokines by myeloid cells, which the

91 insulin resistance, leptin, CRP, IL-1RA, and IL-6, and lower ghrelin than subjects in other groups, a

92 associated with failure to induce IL-23 and IL-6, two key IL-22 inducers in the early and late phase

93 ry cytokines (TNF-alpha, IL-1beta, CCL-3 and IL-6), and reduced oxidative stress (iNOS and NO) in LPS

94 All three elicited IL-8 and IL-6 from monocytes, but B. subtilis PGA also elicited I

95 ts found chitotriosidase enzyme activity and IL-6 to be significant independent predictors for white

96 Chemerin/ChemR23 induced TNF-alpha and IL-6 expression dependent on Erk1/2, p38 MAPK and PI3K-A

97 erine inhibited LPS-stimulated TNF-alpha and IL-6 secretion by primary human monocytes.

98 nflammatory mediators, such as TNF-alpha and IL-6.

99 al tissue cathepsin K, Runx2, TNF-alpha, and IL-6 expression.

100 ced serum levels of IL-1beta, TNF-alpha, and IL-6 were significantly elevated in DUSP11-deficient mic

101 Trypsinogen, procathepsin B, and IL-6 concentrations as well as cathepsin B, myeloperoxid

102 , CD31, and IL-4 with reduction of CCL28 and IL-6 levels associated with improved wound healing.

103 n models were used to assess eosinophils and IL-6 as predictive biomarkers.Measurements and Main Resu

104 in 6 (IL-6) levels surge during exercise and IL-6 favors exercise capacity.

105 ers and expressed BDNF, TGF-beta1, GFAP, and IL-6.

106 reactive protein (hsCRP), and both hsCRP and IL-6 decreased among participants receiving canakinumab

107 w that the crosstalk between osteocalcin and IL-6 is conserved between rodents and humans.

108 T cells was dependent upon NFkappaB-p65 and IL-6 expression in dendritic cells (DCs), as well as ary

109 significantly elevated at presentation, and IL-6, IL-8 and TNF-alpha levels were higher in complicat

110 ce-associated secretory phenotype (SASP) and IL-6 expression.

111 LPS further increased expression of TSPO and IL-6 in SNCA mice.

112 Anti-IL-6 antibodies (SMD = 0.8, 95% CI [0.20-1.41]) and an a

113 We previously reported 3 anti-IL-6 nonresponders with increased mTOR activation who re

114 anti-IL-12/23 remained significant and anti-IL-6 antibodies became a trend after controlling for phy

115 Importantly, therapy inhibiting (anti-IL-6) or mimicking (IGF-1) the cardiac hMSC secretome ca

116 sessed effects of ziltivekimab, a novel anti-IL-6 ligand antibody, in patients on hemodialysis with r

117 To mark the tenth anniversary of anti-IL-6 receptor therapy worldwide, we discuss the history

118 ARS-CoV-2, such that the repurposing of anti-IL-6 therapeutics for COVID-19 is now a major line of in

119 spermidine prevented the increase in aortic IL-6 and Parkin, attenuated mitochondrial dysfunction, a

120 romote microglial phagocytic states, such as IL-6 and IL-4, and increased expression of microglial ch

121 cs include monoclonal antibodies directed at IL-6, the IL-6 receptor (IL-6R), and Janus kinase inhibi

122 BAL correlated with increased plasma and BAL IL-6 and BAL IL-13.

123 We sought to determine whether baseline IL-6 serum levels can predict the need for IMV and the r

124 Because IL-6 is a relevant cytokine in acute respiratory distres

125 f NK cells.CONCLUSIONThe association between IL-6 serum levels and the impairment of cytotoxic activi

126 itoring a panel of five cytokine biomarkers (IL-6, IL-8, IL-10, TRAIL & IP-10), that is attributed as

127 .5 to assign class, inflammatory biomarkers (IL-6, IL-8, and sTNFR-1; P < 0.0001) and 90-day mortalit

128 Blocking IL-6 has been proposed as a promising therapeutic strate

129 nd two distinct mechanisms by which blocking IL-6, CD47 and PD-L1 reversed fibrosis, by increasing ph

130 cit is correctable by osteocalcin but not by IL-6.

131 imulating the JAK/STAT3 signaling pathway by IL-6 trans-signaling mechanisms, so promoting cancer agg

132 ic cells was associated with decreased cAMP, IL-6 and IL-12.

133 scle and that to increase exercise capacity, IL-6 must signal in osteoblasts to favor osteoclast diff

134 In these cells, IL-6 bound to the soluble receptor (sIL6R), stimulating

135 netic means that the majority of circulating IL-6 detectable during exercise originates from muscle a

136 Colonic IL-6 levels as well as substance P and S100beta density

137 ical pathways (TREM1, NF-kappaB, complement, IL-6 signaling) and upstream regulators (INFgamma, IL-1b

138 ddition of reporter nanoparticles containing IL-6 as target protein.

139 in (IgM, IgA and IgG), and cytokine content (IL-6, IL-8, IL-10, and TNF-alpha), and antioxidant activ

140 ated with RM (r = 0.236, p = 0.045), and CSF IL-6 soluble receptor, which correlated with anhedonia (

141 RABL6), cytokines and growth factors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), ATM and p53 signaling pa

142 his to produce the hepatoprotective cytokine IL-6, thereby ameliorating AILI.

143 rexpression of the pro-inflammatory cytokine IL-6.

144 se in the level of the inflammatory cytokine IL-6; and (iii) downregulation of the JAK1, STAT1, NF-ka

145 L-10, but not the pro-inflammatory cytokines IL-6 or IL-21, is required via STAT3 activation to up-re

146 STEMI, except for pro-inflammatory cytokines IL-6, IL-18, and MIG, as well as anti-inflammatory IL-2

147 he expression of pro-inflammatory cytokines (IL-6, IL-1beta, and TNF-alpha) was significantly reduced

148 the expression of proinflammatory cytokines (IL-6, IL-8) in NiV-infected PBEpC was not decreased.

149 athways to produce representative cytokines (IL-6) and chemokines (CXCL-1), respectively.

150 Consistent with in vivo data, IL-6 knockdown by small interfering RNA or the blockade

151 TREK-1 activation also decreased IL-6, IP-10, and CCL-2 secretion from primary AECs.

152 associated with mortality, while decreasing IL-6 levels are associated with recovery.

153 duction of AAMPhi, whereas mast cell-derived IL-6 enhanced macrophage responsiveness to IL-13 via upr

154 ta demonstrate that endothelial cell-derived IL-6 enhances the self-renewal of dental pulp stem cells

155 the one seen in mice lacking muscle-derived IL-6 (mIL-6), and why this deficit is correctable by ost

156 Network analysis also suggested differential IL-6-related inflammatory programs in WT versus IRF3-KO

157 that VR23 not only effectively downregulates IL-6 but also inhibits cell migration.

158 nduced inflammation via mediating downstream IL-6/STAT3 signaling.

159 d COVID-19 pneumonia patients found elevated IL-6 levels correlated with mortality that did not chang

160 zed sprout formation in response to elevated IL-6 levels secreted by tumor myoepithelial (Epi-T) cell

161 ing, we randomized 61 patients with elevated IL-6 (>=4 pg/ml) to receive placebo or ziltivekimab (dos

162 During stress, endocrine IL-6 is the required instructive signal for mediating hy

163 Mechanistically, MAOA enhances IL-6 transcription through direct Twist1 binding to a co

164 ation of IL-6 by administration of exogenous IL-6 ameliorated AILI in HIF-2alpha(mye/-) mice.

165 Finally, IL-6-mediated hepatoprotection against AILI was abolishe

166 bserved in both directions, particularly for IL-6; however, the strength and importance of this relat

167 58Ala coding mutation as a genetic proxy for IL-6 inhibition.

168 the only biologically relevant receptor for IL-6 in mice.

169 nuclear export, with both being required for IL-6-induced MSH3 export.

170 Furthermore, IL-6 and IL-17 levels are lower in patients on anti-CD20

171 The expression levels of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were signif

172 GCF IL-6 and TNF-alpha levels were significantly reduced in

173 7 and Treg-related mediators in the gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-beta and GITR; P

174 High IL-6 level, C-reactive protein level, lactate dehydrogen

175 Patients with high IL-6 not treated with TCZ showed high mortality (hazard

176 The induction of hippocampal IL-6 after pilocarpine SE was nearly abolished in EP2 co

177 trate a previously unrecognized role of host IL-6 response in the regulation of lung inflammation dur

178 mmatory cytokines, including vIL-6 and human IL-6 (hIL-6).

179 leukin-6 (vIL-6) is a viral homolog of human IL-6 (hIL-6) that is expressed in KSHV-associated malign

180 re we report that a cascade involving IFN-I, IL-6 and B cells promotes TH17-mediated neuro-autoimmuni

181 U stay and mortality, whereas improvement in IL-6:AAT was associated with clinical resolution (P < 0.

182 unwell patients with COVID-19, increases in IL-6:AAT predicted prolonged ICU stay and mortality, whe

183 multiple cytokines and chemokines, including IL-6 and IL-8, in response to starvation stress.

184 formation and laboratory findings, including IL-6 levels, were collected approximately 3 and 9 days a

185 of selective inflammatory markers including IL-6, CXCL10, CXCL11, IFNgamma, IL-10, and monocyte-attr

186 Correlating mortality with increased IL-6 doesn't imply causality however lack of improvement

187 IP accelerates atherosclerosis and increases IL-6/IL-1beta expression, raising the hypothesis that IL

188 hich differentially regulates IL-17A-induced IL-6 and CXCL-1 production, is unique.

189 proteins is required for the IL-17A-induced IL-6 levels.

190 , and PAS800-IL-Ra reduced IL-1alpha-induced IL-6 and IL-8 levels with comparable potency.

191 mic activity of compound 42 in a TNF-induced IL-6 mouse model and in vivo activity in a collagen anti

192 l adjustment for biomarkers of inflammation (IL-6, TNF-alpha, high-sensitivity C-reactive protein, fi

193 levels of cytokines reflecting inflammation (IL-6, IFN-gamma, IP-10, IL-1RA, IL-10), chemotaxis (IL-8

194 rticosteroids (<= 2 mg/kg day) could inhibit IL-6 production (a representative of cytokines) as effec

195 Of these, 25u was found to robustly inhibit IL-6-activated signal transducer and activator of transc

196 ion to determine effectiveness of inhibiting IL-6/IL-6R to ameliorate chronic allograft rejection and

197 ide, we discuss the history of research into IL-6 biology and the development of therapies that targe

198 e whether inflammatory pathways that involve IL-6 and TNF-alpha increase susceptibility to infection

199 , neutrophil-to-lymphocyte ratio, LDH level, IL-6 level, and age was developed and showed high accura

200 o, 4.6; P = .003), as well as those with low IL-6 treated with TCZ (hazard ratio, 3.6; P = .016).

201 A significant decrease in GCF and serum LRG, IL-6 and TNF-alpha was detected after periodontal treatm

202 Exacerbated production of cytokines, mainly IL-6, points to macrophages as key to understand differe

203 ly, mRNA levels of pro-inflammatory markers (IL-6, IL-1beta, COX-2 and TNF-alpha) decreased.

204 Maternal IL-6 response negatively correlated with adult offspring

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

206 th C5aR2 activation reducing Mincle-mediated IL-6 and TNF-alpha generation by 80-90%.

207 In an AA model, IL-6 deficiency led to increased lung inflammation, eosi

208 we developed a mouse model, in which murine IL-6 is overexpressed in a CD11c-Cre-dependent manner.

209 nflammatory response including activation of IL-6, and promotes tumorigenesis in vitro and in vivo.

210 uently in DLB and the serum concentration of IL-6 was increased compared with controls.

211 characterized by elevated concentrations of IL-6, TNF-alpha, and C-reactive protein, which has been

212 zumab treatment is supported by detection of IL-6 in pathogenic levels in all patients.

213 everest form has been marked by elevation of IL-6, IL-10, TNF-alpha, and other cytokines and severe C

214 o elevated chemokines and high expression of IL-6.

215 ut nicotine resulted in a 2-fold increase of IL-6 in the cerebellum.

216 Inhibition of IL-6 by its blocking antibody in BMM-OB cocultures dimin

217 sprouting assays revealed that inhibition of IL-6 or STAT3 signaling decreases the vasculogenic poten

218 Interruption of IL-6/JAK/STAT3 pathway by a JAK inhibitor AZD1480 revers

219 Knockout (KO) of IL-6 in muscle lamin A/C-KO mice diminishes the deficits

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

221 The maximal level of IL-6, followed by CRP level, was highly predictive of th

222 tic shock and find that increasing levels of IL-6 and bla(TEM) are associated with mortality, while d

223 asures and had significantly lower levels of IL-6 and IL-13.

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

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

226 8 +/- 1.7 to 25.9 +/- 4.3; and the levels of IL-6 decreased from 46.8 +/- 10.2 to 35.0 +/- 11.9.

227 sferase isoforms and had increased levels of IL-6 signaling intermediates such as IL-6R and signal tr

228 tivation markers and higher plasma levels of IL-6 than did healthy ANA+ European Americans.

229 ) and DHF had significantly higher levels of IL-6, IL-10 and MIP3alpha than those who developed mild

230 ib had a marked reduction in serum levels of IL-6, IL-1beta, and TNF-alpha, a rapid recovery of circu

231 Long-term neutralization of IL-6 or TGF-beta protected TNF(-/-) mice from an otherwi

232 Smad3 and TAK1 proteins; in the presence of IL-6, expression of Smad3 and Foxp3 but not TAK1 decreas

233 t of MK2/3 in mice reduced the production of IL-6 and IL-13 (two cytokines implicated in asthma) but

234 nterleukin-1 (IL-1) blocks the production of IL-6 and other proinflammatory cytokines, we treated COV

235 croenvironment, and observe up-regulation of IL-6 and TGFbeta signalling-induced gene expression in a

236 and metformin, also promoted the release of IL-6 and IL-8.

237 Restoration of IL-6 by administration of exogenous IL-6 ameliorated AIL

238 e that MAOA is down-regulated as a result of IL-6/IL-6R/STAT3 signalling and epigenetic mechanisms, e

239 ay a framework for understanding the role of IL-6 in the context of cancer research and COVID-19 and

240 ren; further studies to evaluate the role of IL-6 in the life course of asthma are needed.

241 We sought to determine the role of IL-6 in the regulation of lung inflammation in murine AA

242 m, and we identify the distinct secretion of IL-6 as the paracrine cause of PI3Kalpha(H1047R)-associa

243 hese results suggest that clinical trials of IL-6 pathway inhibitors in OCCC may be warranted, and th

244 sis pathogenesis via differential impacts on IL-6-related inflammatory programs.

245 al changes were observed in UCH-L1, Iba-1 or IL-6 over 6 h.

246 In addition, when either STAT3 or IL-6 were inhibited in mice, the phenotypes observed in

247 ly reduced in Group 2 compared to control (P(IL-6) =0.01, P(TNF-alpha) =0.02).

248 In ankylosing spondylitis patients, IL-6 and LRG-1 were identified as biomarkers with concor

249 arkers, D-dimer, B-type natriuretic peptide, IL-6, and IL-10 levels were common but not ubiquitous.

250 significant increases in both baboon and pig IL-6 in the baboon serum, especially in baboons that rec

251 All the AGMs had increased levels of plasma IL-6 compared with baseline, a predictive marker and pre

252 ted patients showed reduced levels of plasma IL-6, TNF, IL-1beta, and phosphorylated STAT3 as well as

253 Finally, IFN-I stimulates B cells to produce IL-6 to drive pathogenic TH17 differentiation in vitro.

254 s; also, some lung cells are able to produce IL-6.

255 The mTORC1 inhibitor rapamycin also reduced IL-6 and IL-13 production, which would be consistent wit

256 rs of large CHIP clones, genetically reduced IL-6 signaling abrogated this risk.

257 sistent with a model in which MK2/3 regulate IL-6 and IL-13 via mTORC1 activation in ILC2s.

258 ing sIL-6R and, thus, systemically regulated IL-6 signaling.

259 le lamin A/C to prevent cellular senescence, IL-6 expression, hyperosteoclastogenesis, and trabecular

260 Serum IL-6 was associated with asthma exacerbation risk but no

261 There were no overall differences in serum IL-6, IL-10, C-reactive protein, and length of stay.

262 Sevoflurane increases the level of serum IL-6, which activates STAT3 and the infiltration of CD11

263 gnaling pathways, including NF-kB signaling, IL-6 signaling, LPS/IL-1-mediated inhibition of RXR Func

264 In NMOSD, elevated IFN-I signatures, IL-6 and IL-17 are associated with severe disability.

265 kin-6 (IL-6) trans-signaling via the soluble IL-6 receptor (IL-6R) and robustly support adult neuroge

266 st AILI was abolished in hepatocyte-specific IL-6 receptor knockout mice.

267 Strikingly, IL-6 blockade attenuates disease only in mice treated wi

268 Overall, lactobacilli suppressed IL-6 (adjusted p < 0.001) and IL-8 (adjusted p = 0.0170)

269 eptor signaling complexes with the synthetic IL-6 receptor chain SyCyR(gp130).

270 and the development of therapies that target IL-6 signalling, including the successes and challenges

271 beta expression, raising the hypothesis that IL-6 pathway antagonism in CHIP carriers would decrease

272 rthermore, in agreement with the notion that IL-6 acts through osteocalcin, we demonstrate that mIL-6

273 ger, supporting the recent observations that IL-6 and C-reactive protein could be used as markers for

274 Last, we showed that IL-6 and C-reactive protein serum concentrations were hi

275 monoclonal antibodies directed at IL-6, the IL-6 receptor (IL-6R), and Janus kinase inhibitors.

276 binding to a conserved E-box element at the IL-6 promoter.

277 rectly, with a number of proteins beyond the IL-6 signal transducer, gp130, and can mediate activitie

278 cted against S. pneumoniae lung disease, the IL-6 deficiency abrogated the protective effect of aller

279 This explains why mice lacking the IL-6 receptor only in osteoblasts exhibit a deficit in e

280 inical phenocopies through impairment of the IL-6 and IL-11 response pathways.

281 Moderate-to-severe CRS is managed with the IL-6 receptor antagonist tocilizumab with or without cor

282 was overwhelmed in severe illness, with the IL-6:AAT ratio markedly higher in patients requiring ICU

283 ogen-induced upregulation of IFN-gamma, TNF, IL-6, CXCL9, CXCL10, and IL-1beta production.

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

285 pression of inflammatory cytokines TNFalpha, IL-6, IL-8 or IFNbeta.

286 ffector T cells were additionally exposed to IL-6.

287 Acute exposure of myotubes to IL-6 increased the mitochondrial reactive oxygen species

288 of function and DN for cellular responses to IL-6, IL-11, LIF, and OSM.

289 alysis ranked chitotriosidase as superior to IL-6 in distinguishing good from poor therapeutic contro

290 s hypothesized to heighten susceptibility to IL-6-mediated inflammatory effects.

291 regression model, ISOLD score, and IL-10-to-IL-6 ratio achieved AUCs of 98.3%, 97.7%, and 96.3%, res

292 2%, 95.3%, 95.6%, and 93.9% for the IL-10-to-IL-6 ratio.

293 ase in genetically-predicted log-transformed IL-6 was 0.74 (95% CI 0.62-0.89; p = 0.0012); and per un

294 proteins of the stromal MAOA-induced Twist1/IL-6/STAT3 pathway in clinical specimens.

295 Upon IL-6 treatment, Endo-N and Endo-T cells displayed altere

296 This suggests the possibility of using IL-6 or CRP level to guide escalation of treatment in pa

297 al interleukin-6 (vIL-6) was the first viral IL-6 homologue to be identified.

298 s uveitis and associated aqueous or vitreous IL-6 and IL-10 levels were collected retrospectively.

299 roup 3 innate lymphoid cells (ILCs), whereas IL-6 administration during the late phase rescued IL-22-

300 with DHF had 25-fold higher levels, whereas IL-6 levels were 11-fold higher in those with COVID-19 S