ライフサイエンスコーパス: interleukin-1beta

1 a2) and inflammation (tumor necrosis factor, interleukin 1beta).

2 creased inflammation (including elevation of interleukin-1beta).

3 hat is dependent on Toll-like receptor 2 and interleukin 1beta.

4 resistant to reactivation by vorinostat and interleukin 1beta.

5 he inflammatory factors cyclooxygenase 2 and interleukin 1beta.

6 st revealed a potential publication bias for interleukin 1beta.

7 nd upregulation of pro-inflammatory cytokine interleukin-1beta.

8 ion while still expressing a basal amount of interleukin-1beta.

9 nd release of inflammatory cytokines such as interleukin-1beta.

10 y genes, including tumor necrosis factor and interleukin-1beta.

11 olarizations in POAF subjects in response to interleukin-1beta.

12 with elevated levels of cytokines, including interleukin-1beta.

13 inducible NO synthase, cyclooxygenase-2 and interleukin-1beta.

14 itment toward cellular debris is mediated by interleukin-1beta.

15 ome such as NLRP3, Toll-like receptor 4, and interleukin-1beta.

16 ation, particularly in the production of IL (interleukin)-1beta.

17 9 mumol mg(-1) ; P < 0.01) and inflammation (interleukin-1beta, 226.8 +/- 27.1 vs. 182.5 +/- 21.5 pg

18 active protein (CRP), tumor necrosis factor, interleukin 1beta, 6, and 10, leukocyte telomere length,

19 ased secretion of inflammatory cytokines IL (interleukin)-1beta (98%, P<0.0001) and IL-6 (460%, P<0.0

20 induces caspase-1 activation and release of interleukin-1beta, a pro-inflammatory cytokine involved

21 opathy of prematurity is induced by systemic interleukin-1beta administration, we undertake gene netw

22 The cytokines interleukin 1beta and 6 (IL-1beta, IL-6) mediate the acu

23 rculating levels of the cytokines leptin and interleukin 1beta and decreased peritoneal proinflammato

24 xpression of tumor necrosis factor-alpha and interleukin 1beta and improved liver histology compared

25 is-inducing ligand and induced expression of interleukin 1beta and interleukin 6 messenger RNAs in mo

26 se did not require the autocrine feedback of interleukin 1beta and tumor necrosis factor alpha releas

27 associated with reduced Aspergillus-induced interleukin 1beta and tumor necrosis factor alpha secret

28 tion of inflammatory cytokines including IL (interleukin)-1beta and IL-6.

29 vity was evaluated by measuring the level of interleukin-1beta and -18 in the supernatants of activat

30 nflammasome NLRP3, leading to the release of interleukin-1beta and -18, potent atherogenic cytokines.

31 lammatory state, eliciting the production of interleukin-1beta and -6, leading to increased ROS.

32 o result in a caspase-8-driven activation of interleukin-1beta and a subsequent induction of the brai

33 ive immunization against NeSt1 decreases pro-interleukin-1beta and CXCL2 expression, prevents macroph

34 genase-2 expression and apoptosis, decreased interleukin-1beta and FAS concentrations, and increased

35 nflammatory stress, induced by the cytokines interleukin-1beta and interferon-gamma, leads to citrull

36 es from human pancreatic islets treated with interleukin-1beta and interferon-gamma.

37 generation of the pro-inflammatory cytokines interleukin-1beta and interleukin-18 and pyroptotic cell

38 tion of the NLRP3 inflammasome, secretion of interleukin-1beta and interleukin-18, and pyroptosis.

39 spase-1 and the subsequent release of mature interleukin-1beta and interleukin-18.

40 ukin-1beta did not respond to LPS early, and interleukin-1beta and interleukin-6 fluctuated although

41 Proinflammatory cytokines (interleukin-1beta and interleukin-6) and adenosine triph

42 e processing of the proinflammatory cytokine interleukin-1beta and is implicated in many inflammatory

43 Consequently, HSCs are hyperactivated by interleukin-1beta and possibly other proinflammatory cyt

44 Group EP presented greater levels of interleukin-1beta and receptor activator of nuclear fact

45 of the cytoplasmic inflammasome to increase interleukin-1beta and thus enhance its cellular adhesion

46 inflammation (both: inflammation score; FR: interleukin-1beta and tumor necrosis factor alpha) vs. O

47 d cells key inflammatory response mediators (interleukin-1beta and tumor necrosis factor alpha), whic

48 ater production of the inflammatory cytokine interleukin-1beta and was attenuated in a murine skin an

49 iators, such as tumor necrosis factor alpha, interleukins 1beta and 18, and brain-derived growth fact

50 atory (NLR family pyrin domain containing 3, interleukins 1beta and 6, and cysteine-cysteine chemokin

51 n of cytokines (tumor necrosis factor-alpha, interleukin-1beta) and restored interleukin-6 to control

52 TNF-alpha, interleukin 1beta, and LPS markedly increase P-selectin

53 roinflammatory cytokines (eg, interleukin 6, interleukin 1beta, and tumor necrosis factor alpha) in c

54 of proinflammatory mediators interleukin-6, interleukin-1beta, and CXCL1/2 (C-X-C motif ligand 1/2).

55 lerated with upregulated type I collagen and interleukin-1beta, and downregulated matrix metalloprote

56 pression of inducible nitric oxide synthase, interleukin-1beta, and interleukin 1 receptor antagonist

57 oxide synthase, tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6.

58 locyte-macrophage colony-stimulating factor, interleukin-1beta, and interleukin-7) as well as soluble

59 rospinal fluid tumor necrosis factor -alpha, interleukin-1beta, and interleukin-8 in a temporal manne

60 ation of monocyte chemoattractant protein-1, interleukin-1beta, and interleukin-8 transcripts levels

61 enchymal stromal cells reduced astrogliosis, interleukin-1beta, and monocyte chemoattractant protein-

62 kers, including tumor necrosis factor-alpha, interleukin-1beta, and nitric oxide synthase-2, highligh

63 cantly elevated tumor necrosis factor-alpha, interleukin-1beta, and RANKL in the gingival tissue comp

64 icant and massive increase of interleukin-6, interleukin-1beta, and tumor necrosis factor-alpha in ad

65 a/beta], IL-6 [interleukin 6], and IL-1beta [interleukin 1beta]), and markers of endothelial adhesion

66 eased concentrations of active caspase-1 and interleukin-1beta are related to an increased concentrat

67 Currently approved inhibitors of interleukin-1beta are rilonacept, canakinumab, and anaki

68 Long-term therapy with an antibody targeting interleukin-1beta blockade resulted in regression of PAH

69 ected by the up-regulation of interleukin-6, interleukin-1beta, bone sialoprotein, osteoprotegerin, r

70 necrosis factor alpha, interferon gamma, and interleukin 1beta but increased phagocytosis activity an

71 1- and CD3-positive cells, the production of interleukin-1beta by CD11b- and Iba-1-positive cells, an

72 Acute application of interleukin-1beta caused NLRP3-signaling activation and

73 on (but not NPA) levels of interferon gamma, interleukin 1beta, CCL5/RANTES, and interleukin 10 (IL-1

74 ne marrow-derived macrophages by suppressing interleukin 1beta, CD68, and phagocytosis but not CD208,

75 CCL2 level, decreased interleukin 1alpha and interleukin 1beta cervical concentrations, and a signifi

76 ne aminotransferase, zonula occludens-1, and interleukin-1beta compared with HS/CR alone.

77 Over time, a decrease in osteoprotegerin and interleukin-1beta concentrations in PICF along with an i

78 Y females exhibited inflammation, and plasma interleukin-1beta concentrations were increased in XY fe

79 FLIP (Fas-associated via death domain-like interleukin 1beta-converting enzyme inhibitory protein),

80 ety of rilonacept, an interleukin-1alpha and interleukin-1beta cytokine trap, were studied previously

81 ammatory Thrombosis Outcome Study) targeting interleukin-1beta demonstrated that anti-inflammatory th

82 Interleukin-1beta did not respond to LPS early, and inte

83 arrow reconstitution experiments reveal that interleukin-1beta enhances hematopoietic stem cell proli

84 2 or its downstream effectors, caspase-1 and interleukin-1beta, erases the ability of EpSCs to recoll

85 anonical NF-kappaB signaling induces pro-IL (interleukin)-1beta expression.

86 LRP3) inflammasome activation and downstream interleukin-1beta expression in a dose-dependent manner.

87 ndocytosis, ROS generation and increases pro-interleukin-1beta expression in macrophages.

88 Finally, ANDRO inhibited LPS-induced interleukin-1beta expression through NF-kappaB inhibitio

89 EPA treatment also reduced islet interleukin-1beta expression, a proinflammatory cytokine

90 lso reduced neuro-inflammation by decreasing interleukin-1beta expression, activation of astrocytes,

91 ell proliferation, and attenuated macrophage interleukin-1beta expression.

92 P2X7 and promotes inflammasome assembly and interleukin-1beta expression.

93 its release of the pro-inflammatory cytokine interleukin-1beta from activated microglia, consistent w

94 efficiently inhibit ATP-dependent release of interleukin-1beta from human and murine monocytes by a m

95 ceptor by fractalkine induces the release of interleukin-1beta from microglia, which modulates NMDA s

96 ating, for example, transcription of the IL (interleukin)-1beta gene (IL1B).

97 he treatments also reduced concentrations of interleukin-1beta, granulocyte colony-stimulating factor

98 ivating proinflammatory cytokines, including interleukin 1beta (IL-1beta) and IL-18.

99 d early expression of inflammatory cytokines interleukin 1beta (IL-1beta) and IL-6 by human myeloma m

100 tokines such as tumor necrosis factor (TNF), interleukin 1beta (IL-1beta) and interleukin 6 (IL-6).

101 which leads to the proteolytic maturation of interleukin 1beta (IL-1beta) and pyroptosis.

102 ers: Inducible Nitric Oxide Synthase (iNOS), Interleukin 1beta (IL-1beta) and Tumor Necrosis Factor A

103 Interleukin 1beta (IL-1beta) is critical for the in vivo

104 Interleukin 1beta (IL-1beta) is upregulated following te

105 ndent inflammasome activation, which induces interleukin 1beta (IL-1beta) release and reduces interle

106 gnificant difference was detected: Levels of interleukin 1beta (IL-1beta) were lower in dengue-infect

107 6), tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), and monocyte chemotactic p

108 ytokines induced by infection, specifically, interleukin 1beta (IL-1beta), IL-10, and tumor necrosis

109 cterial burdens, produced significantly more interleukin 1beta (IL-1beta), IL-13, IL-17, IL-22, and K

110 sociated with dramatically reduced levels of interleukin 1beta (IL-1beta), IL-18, and gamma interfero

111 ines, including tumor necrosis factor alpha, interleukin 1beta (IL-1beta), IL-6, and interferon gamma

112 Secretion of interleukin 1beta (IL-1beta), in response to inflammasom

113 cytokines tumor necrosis factor (TNF) alpha, interleukin 1beta (IL-1beta), interleukin 18, and interl

114 nal tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta), intracellular adhesion mol

115 he activation of caspase 1 and production of interleukin 1beta (IL-1beta).

116 l secretion of the pro-inflammatory cytokine interleukin 1beta (IL-1beta).

117 RP3 inflammasome and consequent secretion of interleukin 1beta (IL-1beta).

118 ystals, or ATP lead to the robust release of interleukin-1beta (IL-1B).

119 lammasome, which generates cytokines such as interleukin-1beta (IL-1beta) and cell death by pyroptosi

120 A2 secreted significantly smaller amounts of interleukin-1beta (IL-1beta) and IL-18 and had a defect

121 thereby promoting the secretion of bioactive interleukin-1beta (IL-1beta) and IL-18 and inducing an i

122 aturation of the pro-inflammatory cytokines, interleukin-1beta (IL-1beta) and IL-18, and cell death.

123 irect activation of caspase-1, generation of interleukin-1beta (IL-1beta) and IL-18, and pyroptotic c

124 asome activates caspase-1 and the release of interleukin-1beta (IL-1beta) and IL-18, and several infl

125 ction of essential proinflammatory cytokines interleukin-1beta (IL-1beta) and IL-18.

126 e that cleaves the proinflammatory cytokines interleukin-1beta (IL-1beta) and IL-18.

127 tion and release of proinflammatory cytokine interleukin-1beta (IL-1beta) and macrophage pyroptosis.

128 ctive-oxygen-species-dependent production of interleukin-1beta (IL-1beta) and neutrophil-recruiting c

129 infection or injury leads to the release of interleukin-1beta (IL-1beta) and to pyroptosis.

130 and single BHB administration on hippocampal interleukin-1beta (IL-1beta) and tumor necrosis factor-a

131 The proinflammatory cytokine interleukin-1beta (IL-1beta) attracts leukocytes to site

132 Secretion of the cytokine interleukin-1beta (IL-1beta) by macrophages, a major dri

133 Whether inhibition of interleukin-1beta (IL-1beta) can reduce the consequences

134 mokine (C-C motif) ligand 3 (CCL3) and human interleukin-1beta (IL-1beta) expression was detected in

135 d tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta) gene expression in murine m

136 crevicular fluid (GCF) inflammatory mediator interleukin-1beta (IL-1beta) in patients receiving regul

137 mice, in association with a reduced level of interleukin-1beta (IL-1beta) in serum.

138 oreactivity of the pro-inflammatory cytokine Interleukin-1beta (IL-1beta) in the nucleus tractus soli

139 m patients converge to suggest a key role of interleukin-1beta (IL-1beta) in the pathogenesis of Kawa

140 to the GAS protease SpeB directly activating interleukin-1beta (IL-1beta) independent of the canonica

141 ng synthesis of the proinflammatory cytokine interleukin-1beta (IL-1beta) independently of hyperglyce

142 Interleukin-1beta (IL-1beta) is a highly inflammatory cy

143 The alarm cytokine interleukin-1beta (IL-1beta) is a potent activator of th

144 Interleukin-1beta (IL-1beta) is a proinflammatory cytoki

145 Interleukin-1beta (IL-1beta) is abundant in the tumor mi

146 Interleukin-1beta (IL-1beta) is one of the key pro-infla

147 Interleukin-1beta (IL-1beta) is upregulated in lesional

148 l crevicular fluid (GCF) was quantified, and interleukin-1beta (IL-1beta) levels were determined in G

149 aits with distinct microbial communities and interleukin-1beta (IL-1beta) levels.

150 LPA also induced expression of interleukin-1beta (IL-1beta) mRNA but no significant inc

151 MCC950 reduced interleukin-1beta (IL-1beta) production in vivo and atte

152 ke receptor 2 (TLR2)-dependent signaling and interleukin-1beta (IL-1beta) production relative to 381,

153 between the monoclonal protein and increased interleukin-1beta (IL-1beta) production, although intere

154 ces NLRC4 (NOD-like receptor C4) activation, interleukin-1beta (IL-1beta) production, and host tissue

155 hat avirulent C. burnetii triggers sustained interleukin-1beta (IL-1beta) production.

156 l cells resulted in increased cell death and interleukin-1beta (IL-1beta) production.

157 B, activation of the NLRP3 inflammasome, and interleukin-1beta (IL-1beta) release in CD39-deficient m

158 During pyroptotic cell death, interleukin-1beta (IL-1beta) release occurs through casp

159 We found that the microbiota induces interleukin-1beta (IL-1beta) release upon intestinal inj

160 MCs were responding to interleukin-1beta (IL-1beta) secreted by BECs after infl

161 epeat protein 3) inflammasome activation and interleukin-1beta (IL-1beta) secretion in macrophages.

162 nd forms plasma membrane pores, resulting in interleukin-1beta (IL-1beta) secretion, pyroptotic cell

163 lating lipopolysaccharide and NLRP3-mediated interleukin-1beta (IL-1beta) secretion.

164 ed) conditions and is further augmented upon interleukin-1beta (IL-1beta) stimulation.

165 dies indicate that pro-inflammatory cytokine interleukin-1beta (IL-1beta) that is up-regulated follow

166 lammatory cytokine production in response to interleukin-1beta (IL-1beta), alone and in combination w

167 Interleukin-1beta (IL-1beta), an inflammatory cytokine a

168 ines tumor necrosis factor alpha (TNFalpha), interleukin-1beta (IL-1beta), and interferon gamma (IFNg

169 as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) a

170 asured by cleavage of the enzyme, release of interleukin-1beta (IL-1beta), and pyroptosis in LPS-acti

171 There is a strong link between integrins and interleukin-1beta (IL-1beta), but the specifics of the r

172 on factor NF-kappaB and induce production of interleukin-1beta (IL-1beta), IL-6, and tumor necrosis f

173 nes tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), IL-6, IL-10, and IL-12 by

174 e phase of MIS-C, we observed high levels of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17,

175 igh-sensitivity C-reactive protein (hs-CRP), interleukin-1beta (IL-1beta), IL-6, tumor necrosis facto

176 ke protein (ASC) containing CARD, caspase-1, interleukin-1beta (IL-1beta), interleukin-18 (IL-18), nu

177 tokines tumor necrosis-alpha (TNF-alpha) and interleukin-1beta (IL-1beta), may exacerbate vascular da

178 The expression of mRNAs for Interleukin-1beta (IL-1beta), TNFalpha, and TLR4 were ev

179 Currently, data point to interleukin-1beta (IL-1beta), tumor necrosis factor (TNF

180 ociated signal transduction enzymes, but not interleukin-1beta (IL-1beta), were responsible for media

181 demonstrate that SAA increases the cytokine interleukin-1beta (IL-1beta), which is mediated by Nod-l

182 flammasome, leading to a rapid production of interleukin-1beta (IL-1beta), which sustains neutrophil

183 Caspase-1, also known as interleukin-1beta (IL-1beta)-converting enzyme (ICE), re

184 NLRP3/caspase-1 inflammasome activation and interleukin-1beta (IL-1beta)-dependent insulin resistanc

185 Type I interferon restrains interleukin-1beta (IL-1beta)-driven inflammation in macr

186 n and mevalonate kinase (MVK) cause distinct interleukin-1beta (IL-1beta)-mediated autoinflammatory d

187 Defects in interleukin-1beta (IL-1beta)-mediated cellular responses

188 ated NLRP3 inflammasomes have been linked to interleukin-1beta (IL-1beta)-mediated tumorigenesis in h

189 ore identified and characterized neighboring interleukin-1beta (IL-1beta)-regulated messenger RNA (mR

190 es of HMWHA and decrease catabolic events in interleukin-1beta (IL-1beta)-treated human articular cho

191 and maturation of the inflammatory cytokine interleukin-1beta (IL-1beta).

192 ytes expressed the pro-inflammatory cytokine interleukin-1beta (IL-1beta).

193 r stress, and they trigger the maturation of interleukin-1beta (IL-1beta).

194 with proinflammatory cytokines, specifically interleukin-1beta (IL-1beta).

195 tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta).

196 of caspase-1 and a proinflammatory cytokine, interleukin-1beta (IL-1beta).

197 udes release of the proinflammatory cytokine interleukin-1beta (IL-1beta).

198 e processing of the proinflammatory cytokine interleukin-1beta (IL-1beta).

199 flammasome complex to process cytokines like interleukin-1beta (IL-1beta).

200 tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta).

201 y promoting the paracrine action of secreted interleukin-1beta (IL-1beta).

202 ion and release of the inflammatory cytokine interleukin-1beta (IL-1beta).

203 Notably, genes (IFI16, caspase-1, and interleukin 1beta [IL-1beta]) in the canonical pyroptosi

204 nal immunopathology (neutrophil recruitment, interleukin-1beta [IL-1beta] secretion, and lactate dehy

205 tumor necrosis factor alpha [TNF-alpha], and interleukin-1beta [IL-1beta]) and significantly higher l

206 ory mediators (gamma interferon [IFN-gamma], interleukin-1beta [IL-1beta], IL-6, keratinocyte chemoat

207 ptosis, and proinflammatory gene expression (interleukin-1beta [IL-1beta], tumor necrosis factor-alph

208 expression of proinflammatory cytokines (IL [interleukin]-1beta, IL-6, and TNFalpha [tumor necrosis f

209 pase-1 (CASP1) cleavage, and proinflammatory interleukin 1beta (IL1B) maturation.

210 es (controls) and analyzed expression NLRP3, interleukin 1beta (IL1B, in plasma), and IL18 (in plasma

211 onary epithelial A549 cells, we confirm that interleukin-1beta (IL1B) induces expression of dual-spec

212 hasone-induced repression of MAPKs, 14 of 46 interleukin-1beta (IL1B)-induced mRNAs were significantl

213 cretion of inflammatory cytokines, including interleukins 1beta (IL1B) and 8 (IL8).

214 Conceptus production of a unique interleukin 1beta, IL1B2, temporally increases during th

215 The expression of the M1 marker genes interleukin 1beta (IL1beta) and interleukin 6 (IL6) alon

216 riate analyses adjusting for covariates IL6, interleukin 1beta (IL1beta), and interleukin 1Ralpha (IL

217 y tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL1beta) in patient-derived fibroblas

218 that RBP4 primes the NLRP3 inflammasome for interleukin-1beta (IL1beta) release, in a glucose-depend

219 ssion of NLRP3, active caspase-1, and mature interleukin-1beta in human peripheral blood mononuclear

220 ry cytokines tumor necrosis factor alpha and interleukin-1beta in lungs or other organs.

221 h ATP, led to an activation of caspase 1 and interleukin-1beta in P2X7-competent macrophages.

222 mily pyrin domain-containing 3 inflammasome, interleukin-1beta) in neutrophils suppress granulopoiesi

223 hows that soluble danger signals, among them interleukin-1beta, increase bone marrow hematopoietic st

224 tory protein 2, tumor necrosis factor alpha, interleukin-1beta, inducible nitric oxide synthase, inte

225 or TGF-betaRII was strongly increased in the interleukin-1beta inflamed cremaster.

226 (CANTOS), a randomised trial of the role of interleukin-1beta inhibition in atherosclerosis, with th

227 We tested the hypothesis that the interleukin-1beta inhibitor canakinumab would prevent ho

228 ta suggest that therapy with canakinumab, an interleukin-1beta inhibitor, is related to a dose-depend

229 atory therapy with canakinumab targeting the interleukin-1beta innate immunity pathway could signific

230 The released interleukin-1beta interacts with its receptor (interleuk

231 (qRT-PCR), and the proinflammatory cytokines interleukin 1beta, interferon beta, and RANTES (regulate

232 ealed increased transcriptional induction of interleukin 1beta, interferon beta, and RANTES in ZIKV-i

233 berculosis displayed decreased cytokine (ie, interleukin 1beta, interferon gamma, and interleukin 17)

234 on, as indicated by significant increases in interleukin 1beta, interferon gamma, tumor necrosis fact

235 cytokines/chemokines in the brain, including interleukin-1beta, interferon-gamma, and fractalkine as

236 neonatal cells show defective production of interleukin 1beta, interleukin 10, and monocyte chemoatt

237 ed the large amount of heterogeneity between interleukin 1beta, interleukin 6, and C-reactive protein

238 tion of proinflammatory cytokines, including interleukin 1beta, interleukin 6, and interleukin 8, and

239 terferon gamma, tumor necrosis factor alpha, interleukin 1beta, interleukin 6, and multiple chemokine

240 The cytokines interleukin-1beta, interleukin-12, tumor necrosis factor

241 n = 5, controls n = 10) and higher levels of interleukin-1beta, interleukin-1alpha, interleukin-6, in

242 Level of interleukin-1beta, interleukin-2, interleukin-4, interle

243 mpening of pro-inflammatory cytokines (e.g., interleukin-1beta, interleukin-2, interleukin-6, interle

244 tory cytokines (tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and granulocyte macrop

245 brospinal fluid tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and interleukin-8 leve

246 urvival rate, but reduced levels of systemic interleukin-1beta, interleukin-6, and monocyte chemoattr

247 Methotrexate did not result in lower interleukin-1beta, interleukin-6, or C-reactive protein

248 w-dose methotrexate did not reduce levels of interleukin-1beta, interleukin-6, or C-reactive protein

249 n a dose-dependent increase in CSF levels of interleukin-1beta, interleukin-6, tumor necrosis factor

250 rrier dysfunction, astrocyte activation, and interleukin-1beta, interleukin-6, tumor necrosis factor-

251 gens of red and orange complexes and a lower interleukin-1beta/interleukin-10 ratio than the control

252 n in the tumour microenvironment mediated by interleukin 1beta is hypothesised to have a major role i

253 Interleukin-1beta is a potent pro-inflammatory cytokine

254 rone in mice resulted in elevation of plasma interleukin-1beta levels and vascular abnormalities.

255 d beta2, vascular endothelial growth factor, interleukin-1beta, matrix metalloproteinase-1, versican,

256 stress signals, initiates caspase-1-mediated interleukin-1beta maturation and an inflammatory respons

257 The NLRP3 inflammasome controls interleukin-1beta maturation in antigen-presenting cells

258 duced hyperactivation of caspase-1, enhanced interleukin-1beta maturation, and inflammation.

259 tial for caspase-11-dependent pyroptosis and interleukin-1beta maturation.

260 a, and liver tumor necrosis factor-alpha and interleukin 1beta mRNA were evaluated.

261 female mice, as well as increased VEGFR1 and interleukin-1beta mRNA expression in females, and reduce

262 infected with virus or exposed to IFN-gamma/interleukin-1beta or IFN-alpha.

263 Schwann cells, and neural fibers; increased interleukin-1beta (P = 0.004), tumor necrosis factor-alp

264 o stabilizes the mature caspase-1 to promote interleukin-1beta production and pyroptosis.

265 This metabolite potentiates interleukin-1beta production, resulting in hyperinflamma

266 expression, caspase 1 activity, or IL-1beta (interleukin-1beta) protein expression under in vivo and

267 terleukin-6, tumor necrosis factor-alpha and interleukin-1beta), rebalanced levels of short-chain fat

268 of Myb1 (TOM1), a negative regulator of the interleukin-1beta receptor-1 (IL-1R1).

269 Importance: Anakinra, an interleukin 1beta recombinant receptor antagonist, may h

270 aortic aneurysm formation, neutralization of interleukin-1beta reduced arterial wall stiffness and ha

271 e CNS, Rag1(-/-) mice showed lower levels of interleukin 1beta, reduced microglial proliferation, and

272 Canakinumab, a monoclonal antibody targeting interleukin-1beta, reduces inflammation and cardiovascul

273 roglial activation and inflammasome-mediated interleukin 1beta release that contributes to neuroinfla

274 rreversible NLRP3 inhibitor able to decrease interleukin-1beta release from macrophages.

275 Control of interleukin-1beta release is vital as excessively high s

276 age and activity of caspase-1 and downstream interleukin-1beta release(2).

277 roptosis, as measured by caspase-1-dependent interleukin-1beta release, though this phenotype could b

278 y that inhibits inflammation by neutralizing interleukin-1beta, resulted in a lower rate of cardiovas

279 ure, rho = 0.68, P = 0.04) and inflammation (interleukin-1beta, rho = -0.80, P = 0.009).

280 itro, aldosterone stimulated NLRP3-dependent interleukin-1beta secretion by bone marrow-derived macro

281 triggers robust inflammasome activation and interleukin-1beta secretion by dietary fats.

282 idative stress, inflammasome activation, and interleukin-1beta secretion in macrophages.

283 +) T cells and initiates caspase-1-dependent interleukin-1beta secretion, thereby promoting interfero

284 nflammasome in naive neutrophils and promote interleukin-1beta secretion.

285 d an increase in NLRP3 inflammasome-mediated interleukin-1beta secretion.

286 ges were activated and displayed evidence of interleukin-1beta signaling.

287 Interleukin 6 (SMD 0.88; p=0.0003), interleukin 1beta (SMD 1.42; p=0.045), and interferon ga

288 7F, without effects on interleukin 1alpha or interleukin 1beta, suggesting a disturbance in interleuk

289 An antibody that neutralizes interleukin-1beta suppresses these effects.

290 p110delta exhibited constitutive release of interleukin 1beta that was dependent on MEFV but indepen

291 tory and produce robust amounts of IL-1beta (interleukin-1beta) through the non-canonical caspase-11

292 ytes from TBI + Sp mice had higher levels of interleukin-1beta, tumor necrosis factor-alpha, and reac

293 traumatic brain injury and could not produce interleukin-1beta, tumor necrosis factor-alpha, or react

294 ZDF islets contain elevated levels of CB1R, interleukin-1beta, tumor necrosis factor-alpha, the chem

295 ver, unlike TNF-alpha, the secreted level of interleukin 1beta was not affected by coculture with DPS

296 Plasma interleukin 1beta was significantly elevated by BCAA sup

297 Interleukin-1beta was significantly reduced in the contr

298 icular fluid, bleeding on probing (BOP), and interleukin-1beta were tested (ELISA) at baseline, 2 wee

299 , as well as tumor necrosis factor-alpha and interleukin-1beta, were significantly increased in colon

300 nced expression of the inflammatory cytokine interleukin-1beta, when compared to mice with intact CX3