ライフサイエンスコーパス: IL-1Ra

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

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

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

4 I IFN and interleukin-1 receptor antagonist (IL-1ra).

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

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

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

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

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

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

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

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

13 IL-10, transforming growth factor beta, and IL-1Ra.

14 to be mediated by IFN-dependent induction of IL-1ra.

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

16 known to induce irreversible aggregation of IL-1ra.

17 signaling capability onto a K145D mutant of IL-1Ra.

18 ad similar effects on levels of IL-1beta and IL-1ra.

19 size and immunoreactivity as the commercial IL-1Ra.

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

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

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

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

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

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

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

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

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

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

30 receptor using an IL-1 receptor antagonist (IL-1ra; 50 ng/mL) or inhibition of IL-1beta production u

31 IL-1 receptor antagonist (IL-1Ra), a natural inhibitor of IL-1beta, has been shown

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 on of IL-1 receptor antagonist (IL-Ra); this IL-1Ra acts on pDCs to elevate their IFN-lambda1 output.

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

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

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

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

40 ed the role of conformational flexibility in IL-1ra aggregation and shed light on the nature of struc

41 A nucleation-driven IL-1ra aggregation pathway is proposed, and assumes two

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

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

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

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

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

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

48 , he was ultimately treated with recombinant IL-1Ra, anakinra, and experienced significant clinical i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 reased expression of the receptor antagonist IL-1Ra and the decoy receptor IL-1RII.

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

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

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

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

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

69 elevations in both IL-1 receptor antagonist (IL-1Ra) and the ratio of IL-1Ra to IL-1beta.

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

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

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

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

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

75 Administering IL-1beta elevated IL-1ra, and administering IL-1ra depressed IL-1beta leve

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

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

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

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

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

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

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

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

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

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

86 of human interleukin-1 receptor antagonist (IL-1ra) are strongly denaturant-dependent as evidenced b

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

88 ith human interleukin-1 receptor antagonist (IL-1ra) as a protein aggregation model.

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

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

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

92 a self-antagonizing TGF-alpha-IL-1alpha/beta-IL-1ra autocrine cascade in vitro, and thus identify mul

93 tivity of a coupled TGF-alpha-IL-1alpha/beta-IL-1ra autocrine cascade.

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

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

96 facilitates activity and replacing it by the IL-1Ra beta-turn results in a hybrid protein that folds

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

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

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

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

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

102 for regulating the endogenous production of IL-1Ra by innate immune cells are currently unresolved.

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

104 FNAR1-deficient mice had decreased levels of IL-1ra compared with WT mice.

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

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

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

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

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

110 oncentrations of IL-1beta first increased as IL-1ra decreased, and both then changed in the opposite

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

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

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

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

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

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

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

118 IL-1beta elevated IL-1ra, and administering IL-1ra depressed IL-1beta levels.

119 In vitro, IL-1, and IL-1ra did not affect the proliferation of the uveal mel

120 stent with the capacity of IFNbeta to induce IL-1Ra, elevated baseline IL-1Ra levels were associated

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

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

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

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

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

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

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

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

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

130 2 individual cytokine radioligands, (99m)Tc-IL-1ra-Fc (IF) and (99m)Tc-TNFR2-Fc (TF) (n = 6 each gro

131 Nevertheless, we find that IL-1Ra folds faster than IL-1beta.

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

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

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

135 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

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

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

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

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

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

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

142 retion of interleukin-1 receptor antagonist (IL-1Ra), IL-18, and CCL4.

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

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

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

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

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

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

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

150 ntly increased interleukin-1beta (IL-1beta), IL-1RA, IL-2R, IL-6, IL-8, IL-10, IL-12, IL-13, IL-15, t

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

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

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

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

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

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

157 IL-1Ra immunoreactivity was assessed before and after pr

158 pinal cord impaired locomotion, and infusing IL-1ra improved recovery from glutamate-induced motor im

159 l trials have demonstrated the importance of IL-1Ra in chronic inflammatory diseases, the cellular me

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

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

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

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

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

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

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

167 tein spectral change resembles that seen for IL-1ra in the crystalline state.

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

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

170 ndogenous interleukin-1 receptor antagonist (IL-1ra) in glutamate toxicity following SCI.

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

172 Importantly, blockade of IL-1 signaling by IL-1RA inhibited Th17 differentiation and IL-23-induced

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

174 lities, IL-1beta promotes signaling, whereas IL-1Ra inhibits it.

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

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

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

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

179 aturally occurring antiinflammatory cytokine IL-1Ra (interleukin-1 receptor antagonist).

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

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

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

183 IL-1R antagonist (IL-1Ra) is required for adequate host defense in invasiv

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

185 N activity, the IFNbeta/alpha ratio, and the IL-1Ra level were predictive of the therapeutic response

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

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

188 e spinal cord caused changes in IL-1beta and IL-1ra levels very similar to those produced by contusio

189 IFNbeta to induce IL-1Ra, elevated baseline IL-1Ra levels were associated with better therapeutic ou

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

191 he glutamate-induced changes in IL-1beta and IL-1ra levels.

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

193 tive TGF-alpha and IL-1 receptor antagonist (IL-1ra) ligands and antiproliferative IL-1alpha/beta lig

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

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

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

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

198 odeling transcripts upregulated (arginase-1, IL-1Ra, MMP-12, ADAM8, VEGF, and Clec-7a).

199 g cultures with an IL-1 receptor antagonist (IL-1Ra) modulated the DRlyp/lyp signature (P < 10(-6)),

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

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 We hypothesize that elevating IL-1ra opposes the damage caused by IL-1beta in SCI by r

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

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

208 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

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

210 n vivo exposure to type I IFN, which induced IL-1ra, or administration of IL-1ra reduced TLR9-associa

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

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

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

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

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

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

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

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

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

220 that GSK3 negatively regulates the levels of IL-1Ra produced by LPS-stimulated innate immune cells.

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

222 o augment ERK1/2 activity abrogated enhanced IL-1Ra production by GSK3-inhibited cells.

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

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

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

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

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

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

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

230 IL-1ra protected cultured hepatocytes from IL-1beta-medi

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

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

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

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

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

236 , which induced IL-1ra, or administration of IL-1ra reduced TLR9-associated liver injury; the protect

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

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

239 ent elaboration of IL-1 receptor antagonist (IL-1RA) requires IRS-2-mediated PI3K activity in primary

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

241 1beta], rs1143623; IL-1 receptor antagonist [IL-1ra], rs4251961; IL-10, rs1800871; suppressor of cyto

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 oops, a beta-bulge of IL-1beta and a loop in IL-1Ra that interacts with residue K145 and connects bet

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

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

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

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

262 nature (P < 10(-6)), while administration of IL-1Ra to DRlyp/lyp rats delayed onset (P = 0.007), and

263 eceptor antagonist (IL-1Ra) and the ratio of IL-1Ra to IL-1beta.

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

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

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

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

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

269 IL-1ra treatment in vivo also reduced splenic CD11b(+)Gr

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

271 IL-1Ra treatment reduced seizure susceptibility 2 weeks

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

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

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

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

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

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

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

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

280 IL-1 receptor type I (IL-1RI) signaling, FIV(IL-1Ra) vector was injected into the cisterna magna of C

281 production of the anti-inflammatory cytokine IL-1Ra via its ability to regulate the MAPK ERK1/2 in TL

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

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

284 e beta-trefoil fold characteristic of native IL-1ra was preserved until the unfolding transition regi

285 combinant interleukin-1 receptor antagonist (IL-1ra) was revealed and characterized by spectral probe

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

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

288 Levels of interleukin-1 receptor antagonist (IL-1Ra) were determined in baseline plasma samples using

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

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

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

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

293 IL-1ra, which is produced by LMNCs and hepatocytes, is a

294 -inflammatory effects mediated by endogenous IL-1ra, which regulates the extent of TLR9-induced liver

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 nd interleukin-1 (IL-1) receptor antagonist (IL-1Ra), while suppressing IL-6 production through phosp

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

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