ライフサイエンスコーパス: IL-1

1 IL-1 and TNF-alpha stimulate release of urokinase, which

2 IL-1 antagonists should be investigated as adjunctive tr

3 IL-1 cytokine family members and various inflammasomes m

4 IL-1 family member interleukin 37 (IL-37) has broad anti

5 IL-1 family members are central mediators of host defens

6 IL-1 polymorphism and generalized reinfection are associ

7 IL-1 polymorphism and percentage of sites with PD >6 mm

8 IL-1 receptor appears to be a marker of neutrophilic inf

9 IL-1 receptor signaling via the transcription factors Ah

10 IL-1, TNF-alpha, and estrogen stimulate release of Hsp90

11 IL-1-type cytokines can regulate hepatic steatosis; the

12 at is prevented by genetic deletion of IL-1 (IL-1) receptor or apoptosis-associated speck-like protei

13 The roles of the interleukin 1 (IL-1) and interleukin 18 pathways in host defense are we

14 Within the interleukin 1 (IL-1) cytokine family, IL-1 receptor accessory protein (

15 Interleukin 1 (IL-1) receptor-associated kinases (IRAKs) are serine/thr

16 ion by ELF3 in the context of interleukin 1 (IL-1)-driven inflammatory responses in chondrocytes.

17 Interleukin-1 (IL-1) and the IL-1 receptor (IL-1R) family play an impor

18 nflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha, thereby contribut

19 bined anti-CD3 treatment plus interleukin-1 (IL-1) blockade to reverse new-onset disease in NOD mice.

20 The interleukin-1 (IL-1) family cytokines are cytosolic proteins that exhib

21 some, leading to secretion of interleukin-1 (IL-1) family cytokines, pyroptosis, and control of patho

22 activation and release of the interleukin-1 (IL-1) family members, IL-1beta and IL-18.

23 Interleukin-1 (IL-1) is implicated in numerous pathologies, including m

24 otal proinflammatory cytokine interleukin-1 (IL-1) is increased in CML bone marrow.

25 on of several markers such as interleukin-1 (IL-1) receptor accessory protein (IL1RAP), CD99, T-cell

26 l cells, express a functional interleukin-1 (IL-1) receptor complex and respond with NF-kappaB activa

27 , and to evaluate the role of interleukin-1 (IL-1) signaling as a target for pharmacological interven

28 ppaB signaling in response to interleukin-1 (IL-1) stimulation.

29 d by their ability to release interleukin-1 (IL-1) while maintaining cell viability, endowing these c

30 Interleukin-1 (IL-1), an important proinflammatory cytokine, is suspect

31 mediates the TNFR family and interleukin-1 (IL-1)/Toll-like receptor (TLR) signaling cascades.

32 nflammasome pathways, NLRP3, ASC, caspase 1, IL-1 and IL-18.

33 the expression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

34 the deleterious and tissue-destructive IL-18/IL-1/IL-17A axis represents a novel therapeutic approach

35 mation index ratio of interleukin (IL)-1beta/IL-1 receptor antagonist (ra) using enzyme-linked immuno

36 tor (IL-36R) and a shared subunit, IL-1RAcP (IL-1 receptor accessory protein).

37 Expression of interleukin 23 (IL-23), IL-1 receptor I (IL-1RI), IL-17R, tissue inhibitors of m

38 Secretion of IL-23, IL-1, and TNF-alpha, the cytokines required for terminal

39 ) and confirmed 4 asthma risk regions: 2q12 (IL-1 receptor-like 1 [IL1RL1]), 6p21 (HLA-DQA1), 9p24 (I

40 lammatory agents active against the CRP/IL-6/IL-1 axis, including low-dose methotrexate and colchicin

41 cluding elevations in heat-shock protein 70, IL-1, IL-18, and TNFalpha indicative of a sterile inflam

42 uartile: 49.8/68.3 years; six smokers, and 9 IL-1 positive) were included for analysis, each contribu

43 feration, which can be abolished by ablating IL-1 signaling or depleting its major cellular source, t

44 utoinflammatory disorders caused by abnormal IL-1 signaling.

45 on of pro-inflammatory mediators, TNF-alpha, IL-1 beta, IL-6, MMP-2 and MMP-9 in HCECs exposed to hyp

46 ence suggests that interleukin-18 (IL-18; an IL-1 family cytokine) is elevated in depression and impl

47 ptors (TLRs), macrophages generate IL-33, an IL-1 family member that induces innate immune responses

48 Anakinra, an IL-1 receptor antagonist protein, inhibited BAL TH2/TH17

49 , which activated synovial fibroblasts in an IL-1-dependent manner.

50 a, glycolysis was induced in the lungs in an IL-1-dependent manner.

51 IL-33 is an IL-1 cytokine superfamily member.

52 Mice were treated acutely with an IL-1 receptor antagonist (IL-1Ra; 100 mg/kg, s.c.) or ve

53 In conclusion, treatment with an IL-1 trap improved FMDBA without changing aPWV and reduc

54 s etanercept (TNFalpha inhibitor), anakinra (IL-1 receptor antagonist), prednisone (NFkappaB transloc

55 We compared sequences of IL-1beta and IL-1 receptor antagonist (IL1RN), which is an IL-1beta h

56 ased plasma interleukin (IL)-6, IL-1beta and IL-1 receptor antagonist (R=-0.33 to -0.36, P<0.05).

57 A robust increase in IL-1beta and IL-1 receptor were detected after TBI.

58 RNA against NLRP3, recombinant IL-1beta, and IL-1 receptor antagonist confirmed the role of NLRP3 inf

59 S100A7, S100A8, and S100A9 (S100A7/8/9), and IL-1 receptor-associated kinase 1 (IRAK1) establish a re

60 e consequence of inflammasome activation and IL-1 expression is the upregulation of adhesion molecule

61 ts positively correlated with IL-1 alpha and IL-1 beta and with the proportions of Selenomonas, Prevo

62 eta (IL-1beta), an inflammatory cytokine and IL-1 receptor ligand, has diverse activities in the brai

63 tion factor NF-kappaB in response to FGF and IL-1/TNF, respectively.

64 the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor type II.

65 The Toll-like and IL-1 family receptors play critical roles in innate and

66 f MyD88 post-translational modifications and IL-1-driven inflammation.

67 ysiology of EoE and implicated protease- and IL-1-related activities as putative central pathways in

68 ceptors, IL-1 receptor accessory protein and IL-1 receptor type 1 (IL-1R1), and enhanced sensitivity

69 h subsequent immunoglobulin E responses, and IL-1-receptor-deficient mice failed to induce iBALT form

70 ated with an IL-13-induced TH2 signature and IL-1 receptor-like 1 (IL1RL1) mRNA expression.

71 fore, we elucidated the effects of antenatal IL-1 exposure on postnatal development and investigated

72 and can be suppressed by injections of anti-IL-1 receptor antibody.

73 ng rationale for further exploration of anti-IL-1 strategies to enhance LSC elimination in CML.

74 tingly, patients with CAPS treated with anti-IL-1 drugs display methylation levels similar to those o

75 asome complex, to regulatory agency-approved IL-1-neutralizing biologic drugs.

76 These responses are IL-1 signaling-dependent, but independent of PARP1, whic

77 As IL-1 is clearly linked to key clinical symptoms of acute

78 P-activated MDM was independent of autocrine IL-1.

79 ory effects of MSU crystals were shown to be IL-1-dependent using a caspase-1 inhibitor (inhibits IL-

80 D scores with the lowest levels of IFN-beta, IL-1, and epithelial cytokines.

81 sed in the Tg(CJD) hippocampus, and blocking IL-1 receptor signaling restored normal synaptic respons

82 e inhibitor 101.10, for efficacy in blocking IL-1 actions.

83 ogether, these studies suggest that blocking IL-1 or IL-6 receptors may improve the regenerative capa

84 diators in CML LSC, suggesting that blocking IL-1 signaling could modulate the inflammatory milieu.

85 ymosan-induced arthritis, and methylated BSA/IL-1 arthritis by both prophylactic and therapeutic anti

86 Indeed, neutralization of IL-1 by IL-1 receptor antagonist has recently been shown to pote

87 t is partially dependent on autoinduction by IL-1.

88 l to various signaling pathways initiated by IL-1, IL-18, and toll-like receptors, the precise contri

89 gonists tested but urokinase was released by IL-1, TNF-alpha, and thrombin (positive control), but no

90 monocyte and lymphocyte interleukins (called IL-1 and IL-2, respectively).

91 kines and were predicted to have compromised IL-1-regulated signaling.

92 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly increased in

93 then activates the proinflammatory cytokines IL-1 and IL-18.

94 expression of the proinflammatory cytokines IL-1, IL-6, IL-8, and TNFalpha.

95 correlated with pro-inflammatory cytokines (IL-1, IL-6 and others).

96 actor 7 gene expression and rapidly degraded IL-1 receptor-associated kinase 1 expression in plasmacy

97 ne that YOD1 antagonizes TRAF6/p62-dependent IL-1 signaling to NF-kappaB.

98 rather than IL-36, suggesting that different IL-1 cytokines trigger MyD88 signaling depending on the

99 this viral miRNA activity not only disrupts IL-1 autocrine and paracrine signaling loops that can al

100 derived dendritic cells established distinct IL-1-mediated, innate and Th1-mediated adaptive immune r

101 HTR >50% at baseline and positive for either IL-1 genotype version were at significantly higher risk

102 optimal background therapy to receive either IL-1 trap rilonacept or placebo for 12 weeks.

103 the human recombinant form of the endogenous IL-1 receptor antagonist used to treat rheumatoid arthri

104 These in vitro effects require endothelial IL-1 receptors, shown by immunofluorescence to be expres

105 stimulated with optimal doses of estradiol, IL-1, and TNF-alpha (10 ng/mL) from 15 minutes to 120 mi

106 For example, IL-1 signaling pathway, associated with inflammation and

107 in the interleukin 1 (IL-1) cytokine family, IL-1 receptor accessory protein (IL-1RAcP) is the co-rec

108 Participants positive for IL-1 genotype version 2 exhibited earlier progression (f

109 or p62/Sequestosome-1, which is required for IL-1 signaling to NF-kappaB.

110 Growing evidence supports a role for IL-1 in multiple sclerosis and experimental autoimmune e

111 An important role for IL-1-type cytokines and certain inflammasomes has also b

112 osy and offer a novel therapeutic target for IL-1-dependent diseases.

113 Further, IL-1 triggered IKK/NF-kappaB signaling and induction of

114 the inflammatory cytokines interferon gamma, IL-1, and platelet-derived growth factor-BB, which are n

115 e retaining viability, yet it is unclear how IL-1 can be secreted from living cells.

116 affected biological processes and identified IL-1 cytokines and serine peptidase inhibitors as the mo

117 fication of new therapeutic targets in IFN-, IL-1- and IL-17-mediated diseases.

118 The results implicate IL-1 as an important driver of neonatal morbidity in PTB

119 nding their roles in pathogenesis.IMPORTANCE IL-1 signaling plays an important role in inflammation a

120 ing in life-long improved visual function in IL-1 receptor antagonist-treated OIR animals.

121 This insight into the mechanisms involved in IL-1 release from primary human monocytes highlights maj

122 f various innate immune receptors results in IL-1 receptor-associated kinase (IRAK)-1/IRAK-4-mediated

123 The major inflammatory mediators include IL-1 family members, such as IL-1beta, and the functiona

124 trum of proinflammatory cytokines, including IL-1, IL-36, and the neutrophil chemotaxins CXCL1 and CX

125 severe asthma compared with MMAs, including IL-1 receptor (IL-1R) family and nucleotide-binding olig

126 very likely that other molecules - including IL-1, IL-6, IL-17, RANKL, OPG, and CCL2 - modulate probi

127 ophil-rich inflammatory processes, including IL-1 and members of the IL-36 family.

128 nder these conditions S. typhimurium-induced IL-1 release occurred independently of pyroptosis.

129 ults suggest that targeting the inflammasome/IL-1 pathway in tumor microenvironments may provide a no

130 e that dynamic changes of a pro-inflammatory IL-1 superfamily cytokine, IL-18, and its relationship t

131 Targeting the inflammatory IL-1 response could be used as a potential immunomodulat

132 IL1RAP antibodies that inhibit IL-1 signaling could block these effects.

133 IL-1 receptor antagonist (IL-1RA) inhibited IL-1 signaling in CML LSC and inhibited growth of CML LS

134 monocyte production of the natural inhibitor IL-1 receptor antagonist (IL-1Ra) and shifts production

135 hibits IL-1 maturation) and IL-1Ra (inhibits IL-1 signaling).

136 endent using a caspase-1 inhibitor (inhibits IL-1 maturation) and IL-1Ra (inhibits IL-1 signaling).

137 vestigated whether targeting the interleukin IL-1 pathway could reduce inflammation and tissue hypoxi

138 plays an important inhibitory role in local IL-1- and neutrophil-dependent tissue inflammation as sh

139 e highest levels of the inflammatory markers IL-1, IL-4, IL-13, and thymic stromal lymphopoietin.

140 ipated capacity of megakaryocytes to mediate IL-1-driven systemic inflammatory disease.

141 Of the candidate proinflammatory mediators, IL-1 appears central and is sufficient to trigger fetal

142 lating PGE2 production and signaling, namely IL-1 type I receptor (IL-1RI), COX-2, microsomal prostag

143 Transfer of WT but not IL-1-deficient megakaryocytes restored arthritis suscept

144 In this article, we show that the novel IL-1 family member IL-36gamma was expressed during exper

145 In the absence of IL-1 signaling, we noted an increase in the transcriptio

146 tion persisted with additional activation of IL-1/inhibition of RXR, granulocyte diapedesis/adhesion,

147 The biological activity of IL-1 is tightly regulated by the specific receptor antag

148 We hypothesized that administration of IL-1 (interleukin-1) receptor antagonist (anakinra) coul

149 ystemic responses to acute administration of IL-1 or LPS.

150 in of Cdsn(iep-/-) mice and that blockade of IL-1 signaling suppresses both TSLP and IL-23 expression

151 der that is prevented by genetic deletion of IL-1 (IL-1) receptor or apoptosis-associated speck-like

152 ion in the skin, and therapeutic efficacy of IL-1 blockade in a subset of patients with GPP are viewe

153 iatric brain injury, and provide evidence of IL-1 signaling as a mediator of post-traumatic astroglio

154 y represses ST-dependent innate induction of IL-1 family cytokines and neutrophil chemokines.

155 Unexpectedly, the lack of IL-1 signaling increased the mortality and inflammation

156 a greatly up-regulated the protein levels of IL-1 receptor-associated kinase (IRAK-1) and tumor-necro

157 transcriptionally upregulated by ligands of IL-1 receptor/Toll-like receptor family members via the

158 Indeed, neutralization of IL-1 by IL-1 receptor antagonist has recently been shown

159 d investigating the therapeutic potential of IL-1 blockade in MS.

160 pport further investigation into the role of IL-1 ligands in epidermal repair and innate immune respo

161 We investigated the role of IL-1 signaling during MAV-1-induced encephalitis.

162 ncies, and highlight a key mediating role of IL-1.

163 However, the specific roles of IL-1 elements in host immunity to cutaneous viral infect

164 an interact with ASC to mediate secretion of IL-1 cytokines.

165 -induced activation of TLR2 and secretion of IL-1 may be important therapeutic targets to prevent amy

166 een single nucleotide polymorphisms (SNP) of IL-1 and IL-1R family genes with Vogt-Koyanagi-Harada (V

167 pathway is proposed to be similar to that of IL-1 in that an IL-36R agonist (IL-36alpha, IL-36beta, o

168 with and positively correlated with that of IL-1, the IL-36 family proteins, and CXCL1/8.

169 ession of IL-25 and IL-33 by upregulation of IL-1 receptor-associated kinase 1, transforming growth f

170 ; and 7) two previously reported versions of IL-1 genetic patterns associated with periodontitis seve

171 Increased lethality depended on IL-1 receptor 1 (IL-1R1) signaling but not adaptive immu

172 inflammatory Tregs was largely dependent on IL-1 signaling.

173 Here we review recent developments on IL-1 to IL-38, TNF-alpha, TGF-beta, and interferons.

174 neas, but labeling was reduced and patchy on IL-1 receptor (IL-1R)-knockout mouse corneas (P < 0.05,

175 binant human IL-1beta monoclonal antibody or IL-1 receptor antagonist resulted in a dose- and time-de

176 te for Kawasaki disease vasculitis and other IL-1 mediated inflammatory diseases.

177 As with other IL-1 cytokines, IL-36gamma is expressed as an inactive p

178 As observed with other IL-1 superfamily proteins, the IL-36 members require N-t

179 aneous inflammasome activation and paracrine IL-1 signaling, which is sufficient to cause skin inflam

180 Peripheral IL-1 inhibition using anakinra for 4 weeks does not resu

181 rogression is conditional on proinflammatory IL-1 genetic variations.

182 encephalitogenic Th cells and defines a PTX-IL-1-Bhlhe40 pathway active in EAE.

183 rm assessment of risks in patients receiving IL-1 blocking Abs for treatment of chronic inflammatory

184 r antagonist (IL-1Ra) and the decoy receptor IL-1 receptor type 2 (IL-1R2).

185 kine signaling, including the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor type II.

186 increased expression of the IL-1 receptors, IL-1 receptor accessory protein and IL-1 receptor type 1

187 mune components such as Toll-like receptors, IL-1 receptor-associated kinase/tumor necrosis factor re

188 achieved a complete response to recombinant IL-1 receptor antagonist (anakinra).

189 Treatment with recombinant IL-1 receptor antagonist (IL-1RA) inhibited IL-1 signali

190 found that Trim24(-/-) T cells have reduced IL-1 receptor (IL-1R) expression, are refractory to IL-1

191 K63-branched ubiquitin chains also regulate IL-1-inducible phosphorylation of the P-body component D

192 nsequence, AP1S3-deficient cells up-regulate IL-1 signaling and overexpress IL-36alpha, a cytokine th

193 macrophages, allowing these cells to release IL-1 for several days, by a CD14-dependent process.

194 itis was neutrophil independent but required IL-1 and the platelet/megakaryocyte markers NF-E2 and gl

195 R-146a diminished or enhanced, respectively, IL-1 receptor-associated kinase 1 expression and induced

196 se-inactive TRAF6 mutants partially restored IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pelli

197 terleukin [IL]-1 beta [IL-1beta], rs1143623; IL-1 receptor antagonist [IL-1ra], rs4251961; IL-10, rs1

198 Both IL-1alpha and IL-1beta ligate the same IL-1 receptor (IL-1R) that is present on nearly all cell

199 which is defined by their ability to secrete IL-1 while retaining viability, yet it is unclear how IL

200 Megakaryocytes secreted IL-1 directly and as a component of circulating micropar

201 onal Par2 expression to repress sequentially IL-1 receptor type I and Sema3A expression.

202 In these settings, IL-1 induced IL-22 production from a mixed T helper cell

203 The specific IL-1 cytokine instigating development of FMF and the enz

204 of antiinflammatory molecules, specifically IL-1 receptor antagonist (IL-1Ra).

205 Targeting IL-1 signaling could be a promising therapeutic option f

206 ns that affect IL-22 production by targeting IL-1 activity.

207 of CML LSC following TKI treatment and that IL-1 blockade with IL-1RA enhances elimination of TKI-tr

208 We conclude that IL-1 signaling contributes to maintenance of CML LSC fol

209 n vitro Therefore, our data demonstrate that IL-1 functions as a mitogenic mediator of encephalitogen

210 We did not find that IL-1 blockade with anti-IL-1beta monoclonal antibody or

211 Together, these results indicate that IL-1 signaling is important during MAV-1 infection and s

212 Our studies also suggest that IL-1 signaling contributes to overexpression of inflamma

213 lex nature of encephalitis and suggests that IL-1 has a protective effect for the development of MAV-

214 The IL-1 families of ligands and receptors exhibit similarit

215 The IL-1 family member IL-33 plays a critical role in type 2

216 The IL-1 pathway might contribute to airway neutrophilia and

217 The IL-1 superfamily of cytokines and receptors has been stu

218 The IL-1-induced formation of K63-Ub chains and ubiquitylati

219 Interferons and the IL-1 family of cytokines have important roles in host de

220 s play a key role in peanut allergy, and the IL-1 pathway is involved in the Tfh response to peanut a

221 Interleukin-1 (IL-1) and the IL-1 receptor (IL-1R) family play an important role in t

222 tokines, such as interleukin (IL)-10 and the IL-1 receptor antagonist.

223 hibitory effect on IL-1beta secretion by the IL-1 receptor antagonist anakinra in phagocytes of patie

224 and the inflammasome pathway defined by the IL-1-IL-1R interaction between dendritic cells (DC) and

225 nstrate that a viral miRNA downregulates the IL-1 receptor 1 during EBV infection, which consequently

226 A fibrotic infrapatellar fat pad express the IL-1 receptor and on exposure to IL-1alpha polarize to a

227 mphocytes) but not in mice deficient for the IL-1 receptor.

228 contributes to but is not essential for the IL-1-dependent formation of K63-Ub chains, TAK1 activati

229 ive signal 3 receptor pathways and found the IL-1 family member IL-36R.

230 We identified the IL-1 cytokine network as a downstream effector of IL-31

231 gene expression patterns, we identified the IL-1 receptor 1 (IL1R1) as a direct target of miR-BHRF1-

232 y two common functional polymorphisms in the IL-1 gene cluster, which are associated with the inflamm

233 rtance of specific targeted therapies in the IL-1 signaling blockade.

234 ctivated the LCN2 promoter and increased the IL-1-induced mRNA and protein levels of LCN2, as well as

235 -1R2 deficiency on neutrophils increased the IL-1-induced response of fibroblasts in trans.

236 fumigatus In this study, we investigated the IL-1 family member IL-33 in lung defense against A. fumi

237 his study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r(-/-)) or deficient in IL1-be

238 1 (MAV-1) infection, using mice lacking the IL-1 receptor (Il1r1(-/-) mice).

239 se properties required the engagement of the IL-1 decoy receptor 8 (IL-1R8) and the activation of AMP

240 Human mature IL-33 is a member of the IL-1 family and a potent regulator of immunity through i

241 IL-33 is a member of the IL-1 family capable of inducing mast cell responses and

242 kinase 1 to stimulate the expression of the IL-1 family cytokine IL-36gamma in response to P. gingiv

243 we will discuss the role of cytokines of the IL-1 family in hematological malignancies, chemotherapy-

244 IL-18 is a member of the IL-1 family involved in innate immunity and inflammation

245 These findings indicate that members of the IL-1 family of cytokines use distinct molecular mechanis

246 eport that IL-33 (30 ng/mL), a member of the IL-1 family of cytokines, administered in combination wi

247 Additionally, cytokines of the IL-1 family play an important role in homeostatic as wel

248 Members of the IL-1 family play protective and regulatory roles in immu

249 ion between IL-37, the seventh member of the IL-1 family, and CAD is unknown.

250 36gamma), a recently described member of the IL-1 family, and its immunological relevance in host def

251 -18 and IL-1beta, which are cytokines of the IL-1 family, are synthesized as precursor proteins and a

252 IL-37, a member of the IL-1 family, broadly reduces innate inflammation as well

253 ewly found anti-inflammatory cytokine of the IL-1 family, has both extracellular and intracellular fu

254 eceptor, SIGIRR, or TIR8) is a member of the IL-1 receptor (ILR) family with distinct structural and

255 H2/TH17 cells expressed higher levels of the IL-1 receptor and phospho-p38 mitogen-activated protein

256 LSC demonstrated increased expression of the IL-1 receptors, IL-1 receptor accessory protein and IL-1

257 a-chain receptor-independent cytokine of the IL-1 superfamily that is expressed by endothelial cells

258 An absence of IL-17A or the IL-1 receptor was associated with reduced neutrophil rec

259 lmonary aspergillosis, and in particular the IL-1 axis, drives the development of hypoxia.

260 om animal studies suggest that targeting the IL-1 pathway can significantly ameliorate mucositis and

261 ssibilities of therapeutically targeting the IL-1 pathway in hematological patients.

262 ully treated with therapeutics targeting the IL-1 pathway; however, there are a number of identified

263 ifferentiation in multiple ways and that the IL-1 cytokine network is a major downstream effector of

264 breast cancer, we demonstrate here that the IL-1 receptor antagonist anakinra abrogates IL-22 produc

265 dentified two polymorphisms belonging to the IL-1 gene cluster (IL-1beta and IL-1ra) in strong associ

266 eukin-18 (IL18), a cytokine belonging to the IL-1 superfamily that can induce synthesis of several ot

267 c pro-inflammatory cytokine belonging to the IL-1 superfamily.

268 Isolated sJIA monocytes underexpressed the IL-1 inhibitor aryl hydrocarbon receptor (AHR) at baseli

269 trophilia, and wasting, interfering with the IL-1 pathway might be an attractive treatment strategy i

270 ons in acute-phase hsCRP production with the IL-1 receptor antagonist anakinra and the IL-6 receptor

271 cal effects of IL-1beta are mediated through IL-1 receptor (IL-1R).

272 a and IL-1beta, both of which signal through IL-1 receptor.

273 ry cascade from CRP to interleukin (IL)-6 to IL-1 provides novel therapeutic opportunities for athero

274 uently alters the responsiveness of cells to IL-1 stimuli and changes the cytokine expression levels

275 raining lymph nodes after airway exposure to IL-1 family cytokines or natural allergens.

276 ion, pertussis toxin administration leads to IL-1 receptor type 1 (IL-1R1)-dependent IL-1beta express

277 patients who show only a partial response to IL-1 blockade.

278 tion and marked proliferation in response to IL-1.

279 for CAPS patients with partial responses to IL-1-targeted therapies.

280 type 1 (IL-1R1), and enhanced sensitivity to IL-1-induced NF-kappaB signaling compared with normal st

281 d differentiation response gene 88, and Toll-IL-1 receptor domain-containing adaptor-inducing interfe

282 erferon-independent mechanism involving Toll-IL-1-receptor domain-containing adapter-inducing IFN-alp

283 a coli strains, such as CFT073, express Toll/IL-1 receptor-containing (TIR-containing) protein C (Tcp

284 hermore, we show that the intracellular Toll/IL-1 receptor (TIR) domain of Nv-TLR can interact with t

285 cruitment of the adaptor molecule TRIF (Toll/IL-1 resistance (TIR) domain-containing adapter-inducing

286 NF-kappaB nuclear translocation, IL-1 beta and TNF-alpha gene expression, and protein con

287 enzymes readily cleaved IL-18 and IL-33, two IL-1-related alarmins, as well as the cytokine IL-15, wh

288 n postnatal development and investigated two IL-1 receptor antagonists, the competitive inhibitor ana

289 , comparable in extent to that obtained upon IL-1 receptor blockade.

290 Neonatal therapy using IL-1 receptor antagonist preserves choroid and prevents

291 We examined whether IL-1 signaling contributes to the encephalitis observed

292 However, the exact mechanism by which IL-1 is involved in the generation of pathogenic T cells

293 eeth and implants positively correlated with IL-1 alpha and IL-1 beta and with the proportions of Sel

294 applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, usherin

295 interactions of circulating leukocytes with IL-1- or TNF-activated microvascular endothelial cells (

296 the observed efficacy of rescue therapy with IL-1 blockade in recalcitrant KD, and we identify that r

297 nt proportion of patients and treatment with IL-1 and IL-12 receptor subunit beta 1 (Rb1) antibodies

298 is an important diagnosis as treatment with IL-1 antagonists dramatically improves quality of life f

299 Treatment with IL-1 receptor antagonist reduced hypoxia and slightly, b

300 Treatment with IL-1 significantly increased matrix metalloprotease acti