ライフサイエンスコーパス: IL-1Ra

1 anti-inflammatory IL-1 receptor antagonist (IL-1Ra).

2 retion of interleukin-1 receptor antagonist (IL-1RA).

3 etitive inhibitor, IL-1 receptor antagonist (IL-1Ra).

4 ased circulating levels of IL-1R antagonist (IL-1Ra).

5 pha/beta are controlled by IL-1R antagonist (IL-1Ra).

6 atory and antiatherogenic (such as IL-10 and IL-1rA).

7 ecifically correlated with IL-1R antagonist (IL-1Ra).

8 ules, specifically IL-1 receptor antagonist (IL-1Ra).

9 f IL-1beta and IL-1Ra, resulting in inactive IL-1Ra.

10 form of recombinant IL-1Ra, termed chimeric IL-1Ra.

11 t induces IL-1beta and, with a little delay, IL-1Ra.

12 s responsible for the impaired production of IL-1Ra.

13 induction of the anti-inflammatory cytokine IL-1Ra.

14 menable to partial or complete reversal with IL-1Ra.

15 specific for murine IL-1alpha, IL-1beta, and IL-1RA.

16 CREB abolished the gem-mediated increase in IL-1Ra.

17 nism of cortical neurons via upregulation of IL-1Ra.

18 the PI3K-Akt pathway in the upregulation of IL-1Ra.

19 o/Ala/Ser (PAS) random-coil polypeptide with IL-1Ra.

20 d decreased expression of counter-regulatory IL-1RA.

21 with increased skin expression of TOLLIP and IL-1Ra.

22 locker, minocycline, and IL-1beta antagonist IL-1RA.

23 randomly assigned 22 patients to placebo or IL-1ra (1:1) for 4 weeks; 14 completed the trial.

24 Topical formulations containing 5% IL-1Ra, 1% methylprednisolone, 0.05% cyclosporin A, and

25 (-/-) mice, nor by IL-1 receptor antagonist (IL-1RA; 10 mg/kg).

26 ed acutely with an IL-1 receptor antagonist (IL-1Ra; 100 mg/kg, s.c.) or vehicle.

27 ration of interleukin-1 receptor antagonist (IL-1RA; 112 mug) at the time of surgery was sufficient t

28 lammatory cytokine IL-1 receptor antagonist (IL-1Ra, 16 +/- 1.7 ng/mL, mean +/- SEM).

29 crease in interleukin-1 receptor antagonist (IL-1ra) (5-fold) were observed.

30 those profiles with markers of inflammation (IL-1RA, -6, -8, -10, and -18; macrophage inflammatory pr

31 ha3(+) cells secrete more IL-1alpha and less IL-1RA, a natural IL-1 receptor antagonist.

32 small interfering RNA knockdown of neuronal IL-1Ra abrogated the protective effect of gem against IL

33 ammation can cleave chimeric IL-1Ra and turn IL-1Ra active.

34 by binding the IL-1 receptor (IL-1R) whereas IL-1Ra acts as an antagonist, blocking receptor signalin

35 matory signaling pathways, IL-1R antagonist (IL-1Ra) adheres to the same receptor and inhibits proinf

36 Whether IL-1ra administration improves survival in this populati

37 ted by induction of IL-1ra, and prophylactic IL-1ra administration prevented blistering.

38 The effects of the IL-1 receptor antagonist IL-1ra against the aggressive/invasive MUM2B and the non

39 betes than mice treated with anti-CD3 mAb or IL-1RA alone.

40 Plasma IL-1RA also correlated with % TBSA burn, inhalation inju

41 Strong associations between IL-1ra (an anti-nociceptive cytokine) and mu-opioid rece

42 culating levels of IL-1 receptor antagonist (IL-1RA), an endogenous inhibitor of IL-1beta, has been s

43 ndogenous interleukin-1 receptor antagonist (IL-1Ra), an inflammatory marker, was newly identified as

44 by replacement therapy with the recombinant IL-1Ra anakinra.

45 rescued by administration of the recombinant IL-1Ra, anakinra.

46 activity by treatment with IL-1R antagonist (IL-1Ra; Anakinra) inhibited colitis acceleration in TLR2

47 re demonstrated only after treatment with 5% IL-1Ra and 1% methylprednisolone, and were absent after

48 er positive correlation with lactoferrin and IL-1ra and a stronger negative correlation with Rothia.

49 conditions of genetic deficiency of NLRC4 or IL-1Ra and can be rescued by administration of the recom

50 Serum IL-1Ra and G-CSF levels were also significantly elevated

51 iated signals converge on microglia, as both IL-1Ra and GPIbalpha blockade reversed the production of

52 While IL-1Ra and IL-1beta are structurally homologous, IL-1Ra

53 ses revealed significant binding between PAS-IL-1Ra and IL-1R1, although with a slightly lower affini

54 nors demonstrated variation in expression of IL-1ra and IL-2; WNV-infected donors demonstrated variat

55 is investigation supports salivary levels of IL-1ra and IL-6 as potential indicators for PD changes d

56 IL-1Ra and IL-8 correlated with conjunctival staining (0

57 IL-1Ra and IL-8 in DE3 were 4.4- and 2.1-fold higher tha

58 Among them, IL-1Ra and IL-8 were associated with clinical signs and

59 ensitive myokine targets in skeletal muscle (IL-1ra and IP-10/CXCL10) were identified from a cytokine

60 efficacy of two PAS-IL-1Ra molecules, PAS600-IL-1Ra and PAS800-IL-1Ra (carrying 600 and 800 PAS resid

61 We also studied PAS600-IL-1Ra and PAS800-IL-1Ra for efficacy in monosodium urat

62 ivity in CF could be negatively regulated by IL-1Ra and provide a proof-of-concept evidence that infl

63 Secondly, Pf increased anti-inflammatory IL-1RA and reduced neutrophil degranulation, phagocytosi

64 tive TB cases; the combinations of TNF-alpha/IL-1ra and TNF-alpha/IL-10 achieved correct classificati

65 Both IL-1beta/IL-1Ra and TNF-alpha/IL-10 ratio in Candida hyphae-stimu

66 at sites of inflammation can cleave chimeric IL-1Ra and turn IL-1Ra active.

67 tion markers interleukin-1 receptor agonist (IL-1RA) and high-sensitivity C-reactive protein (CRP) pa

68 eptor antagonists (IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor antagonist (IL-36Ra)), and tw

69 ts >0.40: Interleukin-1 receptor antagonist (IL-1Ra) and IL-8.

70 natural inhibitor IL-1 receptor antagonist (IL-1Ra) and shifts production toward the highly inflamma

71 gulated by the specific receptor antagonist (IL-1Ra) and the decoy receptor IL-1 receptor type 2 (IL-

72 (IL-1beta), and of IL-1 receptor antagonist (IL-1ra), and correlated cytokine levels with cortical ex

73 L-1beta), interleukin 1 receptor antagonist (IL-1Ra), and granulocyte colony-stimulating factor (G-CS

74 , IL-1beta, IL-18, IL-1 receptor antagonist (IL-1RA), and IL-8 levels were determined in SC tape stri

75 in mice receiving IL-1 receptor antagonist (IL-1RA), and in mice given the caspase 1 inhibitor Ac-YV

76 in (CRP), interleukin-1 receptor antagonist (IL-1Ra), and soluble interleukin-6 receptor (sIL-6R).

77 F-alpha), interleukin-1 receptor antagonist (IL-1RA), and transforming growth factor-beta (TGF-beta))

78 nts were combined in a meta-analysis, IL-2R, IL-1RA, and CXCL9 (P = .013, .042, and .0012) were assoc

79 hemotherapy, hepatocyte growth factor, IL-8, IL-1RA, and CXCL9 (P = .015, .048, .004, and .0005) pred

80 we examined relationships between IL-1beta, IL-1ra, and functional measures of the endogenous opioid

81 heart, and that both its natural antagonist, IL-1Ra, and G-CSF are being assessed as treatments for a

82 TNF-alpha, IL-1ra, and IL-10 responses had the greatest ability to

83 er insulin, insulin resistance, leptin, CRP, IL-1RA, and IL-6, and lower ghrelin than subjects in oth

84 tosis; IP-10 and thrombocytopenia; HGF, MIG, IL-1RA, and marked splenomegaly; and IL-1RA, IL-2R, IP-1

85 centrations of the antiinflammatory cytokine IL-1Ra, and mediators that drive epithelial repair (MMP-

86 A549 lung carcinoma cells, anakinra, PAS600-IL-1Ra, and PAS800-IL-Ra reduced IL-1alpha-induced IL-6

87 ffects of IL-6 were mediated by induction of IL-1ra, and prophylactic IL-1ra administration prevented

88 ts target, IL-1R1, 85-fold more tightly than IL-1Ra, and this increase translates to an approximately

89 F-alpha], interleukin-1 receptor antagonist [IL-1RA], and transforming growth factor-beta [TGF-beta])

90 were treated with IL-1 receptor antagonist (IL-1RA), anti-IL-1beta, or recombinant IL-1beta.

91 Inhibition of IL-1beta signaling with IL-1RA, anti-IL-1beta, or NLRP3 KO increased RV-induced

92 ptor (IL-1R1), and IL-1 receptor antagonist (IL-1Ra) are all important regulators of the IL-1 signali

93 Patients in the IL-1ra arm had a 53% reduction in mean hsCRP compared wi

94 These results validate PAS-IL-1Ra as an active IL-1 antagonist with marked in vivo

95 in IL-1beta, versus a conserved cysteine in IL-1Ra at the analogous position, 116.

96 Transected rat MCLs received PBS or IL-1Ra at the time of surgery.

97 d higher levels of IL-1 receptor antagonist (IL-1Ra) at all time points leading up to first-time MI,

98 blocker minocycline and IL-1beta antagonist IL-1RA attenuated CO2-evoked freezing.

99 Thus, manipulation of the TLR7-type I IFN-IL-1ra axis may be a new therapeutic strategy for the tr

100 n is negatively regulated by the IL-22/NLRC4/IL-1Ra axis.

101 etreatment with equimolar anakinra or PAS800-IL-1Ra before MSU challenge similarly reduced inflammato

102 aturally-occurring IL-1 receptor antagonist (IL-1Ra) binds and blocks the IL-1 receptor-1 (IL-1R1), p

103 tly, in vivo intervention with a recombinant IL-1Ra blocked IL-1 signaling and markedly attenuated al

104 ine ligand 1 in blood or brain, but systemic IL-1RA blocked LPS-induced cognitive deficits, and syste

105 on of IL-1beta or treatment with recombinant IL-1RA both rescued IFNAR-deficient mice from poly(I:C)-

106 asts, and IL-10(+) and dual-positive IL-10(+)IL-1RA(+) Breg cells significantly correlated with impro

107 c B cells, plasmablasts, and IL-10(+) and/or IL-1RA(+) Breg cells.

108 hese data suggest that M. leprae upregulates IL-1Ra by a TOLLIP-dependent mechanism.

109 nd abrogation of gem-induced upregulation of IL-1Ra by inhibitors of PI3K and Akt indicate a role of

110 S-IL-1Ra molecules, PAS600-IL-1Ra and PAS800-IL-1Ra (carrying 600 and 800 PAS residues, respectively)

111 y macrophage signature (interleukin [IL]-10, IL-1RA, CD163, scavenger and C-type lectin receptors) an

112 re independently associated with circulating IL-1RA concentration (rs4251961 at the IL1RN locus [n =

113 identify genetic determinants of circulating IL-1RA concentration and to investigate their associatio

114 ciated with a significant increase in plasma IL-1Ra concentrations (p = 0.01) during the acute illnes

115 Plasma IL-1Ra concentrations were significantly higher in nonsu

116 IL-1beta/IL-1ra decreased a significant 61% (P = 0.009) only in S

117 for a known mutation (E77X) associated with IL-1Ra deficiency and a novel mutation in exon 2 of the

118 mice and humans occurred under conditions of IL-1Ra deficiency and was rescued in mice by replacement

119 His case highlights IL-1Ra deficiency as an autoinflammatory disease that is

120 Interleukin-1 receptor antagonist (IL-1Ra) deficiency is a rare autoinflammatory disease in

121 role of IL-1Ra has been well demonstrated in IL-1Ra-deficient mice.

122 However, in IL-1Ra-deficient or overexpressor transgenic mice inocul

123 scrapie, neither loss nor overexpression of IL-1Ra demonstrated any observable effect on gliosis, pr

124 PAS600-IL-1Ra displayed markedly extended blood plasma levels 3

125 t effectively shields newborn mice from BPD, IL-1Ra emerges as a promising treatment for a currently

126 Ra and IL-1beta are structurally homologous, IL-1Ra engages only two of the three extracellular domai

127 ng TKI treatment and that IL-1 blockade with IL-1RA enhances elimination of TKI-treated CML LSC.

128 The proportion of the variance in IL-1RA explained by both SNPs combined was 2.0%.

129 IL-1Ra-expressing constructs produced nearly 1 microg/mL

130 dia of eGFP-expressing constructs but not in IL-1Ra-expressing constructs.

131 on of TLR7 significantly increased IFNa4 and IL-1ra expression in the liver.

132 wever, both pathways activate CREB to induce IL-1Ra expression.

133 ammatory IL-10 and IL-1 receptor antagonist (IL-1Ra) expression in mouse liver, human HepG2 cells, an

134 2 individual cytokine radioligands, (99m)Tc-IL-1ra-Fc (IF) and (99m)Tc-TNFR2-Fc (TF) (n = 6 each gro

135 We also studied PAS600-IL-1Ra and PAS800-IL-1Ra for efficacy in monosodium urate (MSU) crystal-in

136 EBI-005 preserves the affinity bias of IL-1Ra for IL-1R1 over the decoy receptor (IL-1R2), and,

137 he value of intracisternal administration of IL-1RA for therapeutic purposes.

138 ckade of IL-1 with IL-1 receptor antagonist (IL-1Ra) fully reversed infection-induced exacerbation of

139 vels of IL-6, IL-8, TNF-alpha, IL-10, MCP-1, IL-1ra, G-CSF, and IL-1beta in carriers of TLR5(1174T) c

140 protein D, matrix metalloproteinase (MMP)-9, IL-1Ra, granulocyte-macrophage colony-stimulating factor

141 The role of IL-1Ra has been well demonstrated in IL-1Ra-deficient mi

142 Curiously, the related IL-1Ra has therapeutic effects in some of these latter p

143 r-lasting alternative, PASylated IL-1Ra (PAS-IL-1Ra) has been generated by in-frame fusion of a long,

144 The IL-1 receptor antagonist (IL-1Ra) has emerged as a pivotal player in the defense a

145 Two biomarkers, IL-1ra (hazard ratio [HR] 1.28, 95% CI 1.03-1.59) and t-

146 n, renin, interleukin-1 receptor antagonist [IL-1ra], hepatocyte growth factor, fatty acid-binding pr

147 5) in Groups 2 and 3: EGF, FGF-2, IFNalpha2, IL-1RA, HSA, keratin-6, and involucrin; cortisol was sig

148 whereas three other isoforms (intracellular IL-1Ra [icIL-1Ra] 1, 2, and 3) are supposed to remain in

149 Blood concentrations of interleukin 1ra (IL-1ra), IL-6, and gamma interferon (IFN-gamma) increase

150 ecting inflammation (IL-6, IFN-gamma, IP-10, IL-1RA, IL-10), chemotaxis (IL-8), systemic and vascular

151 MSC is mediated by a combination of elevated IL-1ra, IL-10, and PGE(2), anti-inflammatory Th2 cytokin

152 Blocking IL-1ra, IL-10, and PGE(2), but not IL-6, heme oxygenase-

153 mmunosuppression was accompanied by elevated IL-1ra, IL-10, and PGE(2).

154 MP-8, MMP-9, OPN, PF4, SDF-1) and cytokines (IL-1ra, IL-16) in BM Soup.

155 In contrast to IL-1Ra, IL-1R2 appears to be less crucial for systemic r

156 (IP-10), tumor necrosis factor (TNF)-alpha, IL-1ra, IL-2, IL-13, and MIP-1beta (macrophage inflammat

157 F, MIG, IL-1RA, and marked splenomegaly; and IL-1RA, IL-2R, IP-10, MIP-1beta, and JAK2V617F.

158 beta, and IL-36gamma), receptor antagonists (IL-1Ra, IL-36Ra), and 2 anti-inflammatory cytokines (IL-

159 ta, IL-36gamma), three receptor antagonists (IL-1Ra, IL-36Ra, IL-38), and an anti-inflammatory cytoki

160 ally significant dysregulation of IFN-gamma, IL-1RA, IL-6, IL-10, IL-19, monocyte chemoattractant pro

161 crosis factor-alpha, interleukin (IL)-1beta, IL-1RA, IL-6, IL-8, IL-10, IL-17,macrophage inflammatory

162 Briefly, plasma concentrations of IL-1RA, IL-6, IL-8, IL-15, eotaxin, and monocyte chemota

163 in the blood and in the lungs, most notably, IL-1RA, IL-6, IL-8, IP-10, and monocyte chemoattactant p

164 L-6 and IL-8 secretion, and decreases in the IL-1Ra/IL-1beta ratio.

165 ammatory (interleukin 1 receptor antagonist [IL-1RA], IL-6) cytokines than vaccination with Ad5 on da

166 ignaling (interleukin-1 receptor antagonist [IL-1Ra], IL-6, IL-8, macrophage inflammatory protein-1 b

167 IL-1Ra in DE2 was 2.3-fold higher than in DE1 (P = 0.038

168 In conclusion, the administration of IL-1ra in MHD patients can lower biomarkers of inflammat

169 way in mediating gem-induced upregulation of IL-1Ra in neurons and suggest gem as a possible therapeu

170 wering drug, in increasing the expression of IL-1Ra in primary mouse and human neurons.

171 and pronounced increase in the expression of IL-1Ra in primary mouse cortical neurons.

172 FN, while Kupffer cells (KCs) mainly produce IL-1ra in response to type I IFN.

173 Furthermore, the long-lasting presence of IL-1RA in the brain (4 d) compared with in the blood (<2

174 the secretion of anti-inflammatory cytokine IL-1RA in the LPS-activated macrophages.

175 s incubation of an IL-1 receptor antagonist (IL-1ra) in EAE slices reduced spontaneous EPSC alteratio

176 nging to the IL-1 gene cluster (IL-1beta and IL-1ra) in strong association with ACLF.

177 t with recombinant IL-1 receptor antagonist (IL-1RA) inhibited IL-1 signaling in CML LSC and inhibite

178 Inhibiting IL-1 with IL-1ra inhibits tumor growth in vivo but not in vitro.

179 e-1 inhibitor (inhibits IL-1 maturation) and IL-1Ra (inhibits IL-1 signaling).

180 Interleukin-1Ra (IL-1Ra) inhibits CXCL8 release from cocultures and reduc

181 ion results showed a significant increase in IL-1RA (interleukin 1 receptor antagonist) mRNA expressi

182 nistration of the anti-inflammatory cytokine IL-1Ra (interleukin 1-specific receptor antagonist).

183 susceptibility to Mtb, and demonstrate that IL-1Ra is an important mediator of type I IFN-driven sus

184 Therefore, upregulation of IL-1Ra is considered important in attenuating inflammati

185 Topical treatment with IL-1Ra is effective in ameliorating the clinical signs o

186 te that the combination of anti-CD3 mAb with IL-1RA is synergistic in reversal of diabetes through a

187 h encodes interleukin-1 receptor antagonist (IL-1Ra), is sufficient to reverse IFN-driven susceptibil

188 Anakinra, a recombinant form of IL-1Ra, is used to treat a spectrum of inflammatory dise

189 One IL-1Ra isoform is secreted, whereas three other isoforms

190 volume had a negative correlation with serum IL-1RA level (P= .012) and a positive correlation with s

191 In conclusion, we show that circulating IL-1RA levels are predicted by two independent SNPs at t

192 IL-2R levels increased in schizophrenia; and IL-1RA levels in bipolar mania decreased.

193 wer peak viremia and lower IL-15, IL-18, and IL-1Ra levels, compared with controls (P < .05; Wilcoxon

194 Serum interleukin 1 receptor antagonist (IL-1RA) levels were elevated in patients with a good out

195 and IL1F10 loci and that genetically raised IL-1RA may be protective against the development of insu

196 ce on most of the healing components tested, IL-1Ra may have greater therapeutic potential with susta

197 Overall, IL-1Ra may have therapeutic potential early in the heali

198 Topical IL-1Ra may hold promise as a novel therapeutic strategy

199 These results support the concept that IL-1Ra modulates MCL-localized granulation tissue compon

200 Here, we compared the efficacy of two PAS-IL-1Ra molecules, PAS600-IL-1Ra and PAS800-IL-1Ra (carry

201 anscriptional level rather than an increased IL-1Ra mRNA stability.

202 e had upregulated expression of IL-1beta and IL-1RA mRNA.

203 recombinant human IL-1 receptor antagonist (IL-1ra) on biomarkers of inflammation and nutrition in M

204 luence of interleukin-1 receptor antagonist (IL-1Ra) on MCL healing.

205 Subjects randomized to EPA with 'high' IL-1ra or hs-CRP or low adiponectin ('high' inflammation

206 alpha), while corresponding associations for IL-1RA or TGF-beta were non-significant.

207 alpha), while corresponding associations for IL-1RA or TGF-beta were nonsignificant.

208 plasma levels of IL-6 and TNF-alpha, but not IL-1RA or TGF-beta, were significantly associated with i

209 Pups were treated daily with IL-1Ra or vehicle for up to 28 d.

210 ence interval [CI], 0.13-0.89; P < 0.05) and IL-1ra (OR, 0.58; 95% CI, 0.35-0.95; P < 0.05) under the

211 We observed a strong positive association of IL-1RA [OR 1.37; 95% CI (1.09, 1.73)] with adult-onset a

212 Ab with or without IL-1 receptor antagonist (IL-1RA), or anti-IL-1beta mAb.

213 IL-1alpha neutralizing antibody, recombinant IL-1RA, or IL-1 receptor-targeting small interfering RNA

214 s with M. leprae produced significantly less IL-1Ra (P < .001), compared with control.

215 was observed after topical treatment with 5% IL-1Ra (P < .01), 1% methylprednisolone (P < .01), and 0

216 -1), IFN-gamma, interleukin (IL)-6, IL-8 and IL-1ra (P < 0.05).

217 rs demonstrated that, at baseline, increased IL-1ra (P = 0.004) and IL-6 (P = 0.009) were significant

218 IL-12 and interleukin 1 receptor antagonist (IL-1RA) (P = .005 and .02) were associated with a shorte

219 nors demonstrated variation in expression of IL-1ra, P-Selectin, IL-4 and IL-5; ZIKV-infected donors

220 nors demonstrated variation in expression of IL-1ra, P-Selectin, IL-4, RANK-L, CD40L and C3a.

221 IL-1Ra partially rescued the immune cell population in h

222 eate a longer-lasting alternative, PASylated IL-1Ra (PAS-IL-1Ra) has been generated by in-frame fusio

223 measurement of six biomarkers (IL-6, nCD64, IL-1ra, PCT, MCP1, and G-CSF) yielded the same predictiv

224 Injecting the same dose of IL-1RA peripherally failed to have a protective effect.

225 IL-1Ra prevented this structural disintegration at 65%,

226 lammatory interleukin-1 receptor antagonist (IL-1Ra) prevents murine BPD.

227 ts, and IL-10- and IL-1 receptor antagonist (IL-1RA)-producing Breg cells were investigated and corre

228 frequency of plasmablasts and IL-10- and/or IL-1RA-producing Breg cells was greater among responders

229 ficient mice displayed both a severe lack of IL-1RA production and an increased production of proinfl

230 a, vascular endothelial growth factor-A, and IL-1RA production in BAL fluid.

231 s been shown to be associated with decreased IL-1Ra production in healthy adults.

232 I IFN, which in turn induces antifibrogenic IL-1ra production in KCs.

233 n vivo data, IFN-alpha significantly induced IL-1ra production in primary KCs.

234 irectly linking the deregulated IL-1beta and IL-1RA production to liver pathology.

235 nd correlates with defective NLRC4-dependent IL-1Ra production.

236 d maintaining a balance between IL-1beta and IL-1RA production.

237 ces IL-1beta secretion but severely inhibits IL-1Ra production.

238 ddition, antibody-mediated neutralization of IL-1Ra provided therapeutic benefit to Mtb-infected B6.S

239 The IL-1RA-raising allele of rs6759676 was also associated w

240 IL-1RA-raising alleles of both SNPs were associated with

241 the inflammation: imbalance in the IL-1beta/IL-1Ra ratio is implicated in many human diseases and ma

242 Furthermore, IL-1beta/IL-1ra ratio was significantly higher in the CSF of acti

243 tive WT mice, and treatment with recombinant IL-1ra reduced liver fibrosis.

244 We demonstrate that chimeric IL-1Ra reduces IL-1-mediated inflammation in vitro and i

245 SA burn, and inhalation injury grade, plasma IL-1RA remained significantly associated with mortality

246 IL-1Ra responses following TLR1/2 (Pam3CYSK4) stimulatio

247 on of the N-terminal peptide of IL-1beta and IL-1Ra, resulting in inactive IL-1Ra.

248 1beta], rs1143623; IL-1 receptor antagonist [IL-1ra], rs4251961; IL-10, rs1800871; suppressor of cyto

249 Remarkably, IL-1Ra secretion is fully restored by treatment with ant

250 IL-1Ra secretion is restored by exogenous antioxidants t

251 cytokine interleukin-1 receptor antagonist (IL-1Ra) secretion in LPS-activated mouse peritoneal macr

252 Of these, IL-1RA seemed to have the strongest correlation with inj

253 received a combination of anti-CD3 mAb with IL-1RA showed a more rapid rate of remission of diabetes

254 AE mice treated with intracerebroventricular IL-1ra showed normal glutamatergic and GABAergic transmi

255 1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and IL-1RA significantly correlated with disease severity.

256 5 days post-administration, PAS800-IL-1Ra significantly reduced leukocyte influx and inflam

257 Our findings suggest that the IL-1Ra single-nucleotide polymorphism rs4251961 plays a

258 ulting dual-domain cytokine ligand, TNFR2-Fc-IL-1ra, specifically binds to TNF and to the type I IL-1

259 f IL-36Ra antagonism is analogous to that of IL-1Ra, such that IL-36Ra binds to IL-1Rrp2 and prevents

260 ient mice displayed an increased circulating IL-1Ra, suggesting a protective role of PDE4B inactivati

261 regression suggested a risk model including IL-1ra, t-PA, and the Framingham Offspring Study T2D sco

262 At 6 months, IL-1Ra-TBI mice had fewer evoked seizures compared with

263 In a chronic study, IL-1Ra-TBI mice showed improved spatial memory at 4 mont

264 e development of a novel form of recombinant IL-1Ra, termed chimeric IL-1Ra.

265 kinetic profile of (99m)Tc-labeled TNFR2-Fc-IL-1ra (TFI) for imaging inflammatory response in an isc

266 cytokine interleukin-1 receptor antagonist (IL-1RA) that could be assigned to liver-infiltrating cel

267 infected mice deficient in or overexpressing IL-1Ra, there was no observable effect on gliosis, PrPre

268 To elucidate the protective role of IL-1RA, this study aimed to identify genetic determinant

269 and chemokines, such as IL-1alpha, IL-1beta, IL-1ra, TNF-alpha, IL-10, G-CSF, and GM-CSF, were less i

270 s IL-36Ra, similar to the ratio required for IL-1Ra to inhibit IL-1beta.

271 cytokines, in particular, IL-1R antagonist (IL-1Ra), to ensure the correct development and outcome o

272 ized two IL-1 receptor ligands, IL-1beta and IL-1Ra, to create an optimized receptor antagonist, EBI-

273 ucible lentiviral vectors containing eGFP or IL-1Ra transgenes were immobilized to the PCL to transdu

274 Using IL-1Ra-treated mice as well as 3 mouse models deficient

275 IL-1ra treatment in vivo did not affect tumor-derived IL

276 IL-1Ra treatment reduced seizure susceptibility 2 weeks

277 In vivo, IL-1ra treatment resulted in substantial growth inhibiti

278 The IL-1beta/IL-1Ra unbalance after activation of multiple TLRs depen

279 or Nfe2l2 RNA silencing prevented IL-10 and IL-1Ra up-regulation, and HO-1 induction failed post-LPS

280 ng constructs produced nearly 1 microg/mL of IL-1Ra upon controlled induction with dox.

281 the endogenous IL-1beta receptor antagonist IL-1Ra upon four-allele loss.

282 PDE4-deficient macrophages revealed that the IL-1Ra upregulation elicited by LPS alone is PKA-indepen

283 tivation is not entirely responsible for the IL-1Ra upregulation in PDE4B-deficient macrophages.

284 However, the single dose of IL-1Ra used in this study was insufficient to maintain t

285 ected with HSV, the ratio of CSF IL-1beta to IL-1RA was associated with a worse outcome (P= .009); a

286 mily cytokines; higher baseline IL-1beta and IL-1ra was identified in females with lower neuroticism.

287 cally administered IL-1 receptor antagonist (IL-1RA) was protective against, and systemic IL-1beta re

288 ession of interleukin-1 receptor antagonist (IL-1ra) was suppressed in TLR7- or IFNAR1-deficient mice

289 ng up to first-time MI, and higher levels of IL-1Ra were associated with an approximately 1.5-fold in

290 Estimates for IL-1Ra were inconsistent among instruments, and pooled e

291 NFR2) and interleukin-1 receptor antagonist (IL-1ra) were fused to the Fc portion of IgG1 using recom

292 L-2R), and one cytokine receptor antagonist (IL-1RA) were significantly increased in acutely ill pati

293 ent for TNF-alpha, sTNFR1, sIL-2R, IL-6, and IL-1RA, whereas it was absent for IL-4 and IL-10.

294 of the naturally occurring IL-1R antagonist (IL-1Ra), which blocks IL-1R1, is broadly used to treat a

295 d production of the IL-1 receptor antagonist IL-1Ra, which restrained NLRP3 activity.

296 e tested the possible role of the endogenous IL-1Ra, which was increased at 70 days p.i.

297 UA also enhanced the synthesis of IL-1ra, while OA suppressed the level of I-TAC.

298 -1alpha, IFN-gamma, LTB-4, MMP-8 and -9, and IL-1Ra with more than 60% (p < 0.05 for all) reduced the

299 Importantly, the combination of IL-1RA with TKI resulted in significantly greater inhibi

300 R3-Tg mice displayed higher levels of IL-10, IL-1ra, Ym1, and arginase activity, whereas the expressi