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 axis-related inflammation signaling may represent a

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

4 IL-1 induced recruitment of IRAK2 Myddosome to mitochond

5 IL-1 induces the alveolar epithelium to produce granuloc

6 IL-1 polymorphism and generalized reinfection are associ

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

8 IL-1 receptor signaling via the transcription factors Ah

9 IL-1 signaling in both dermal gammadelta T cells and oth

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

11 IL-1-stimulated T/C-28a2 cells treated with an A2AR agon

12 We found that the type 1 IL-1 receptor (IL-1R1) is highly expressed in the mouse

13 e measured soluble markers of interleukin 1 (IL-1) activation at 4 different time points before the c

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

15 ue to their low expression of interleukin 1 (IL-1) receptor 1 and high expression of the decoy recept

16 studied the role of the Toll/interleukin 1 (IL-1) receptor adapter and major inflammatory mediator m

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

18 ge inflammatory signaling and interleukin 1 (IL-1) signaling, which attenuates the acute inflammatory

19 sponsive element (IRE) and an interleukin-1 (IL-1) acute box element.

20 d a "cytokine storm." Because interleukin-1 (IL-1) blocks the production of IL-6 and other proinflamm

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

22 th elevated cytokines such as interleukin-1 (IL-1) in the circulation and tissues.

23 Interleukin-1 (IL-1) is a key mediator of inflammation and immunity.

24 Forty years after its naming, interleukin-1 (IL-1) is experiencing a renaissance brought on by the gr

25 tory cytokines in response to interleukin-1 (IL-1) or tumor necrosis factor alpha (TNFalpha) stimulat

26 report that disruption of the interleukin-1 (IL-1) pathway completely uncouples the SASP from other s

27 Further, we show that lack of interleukin-1 (IL-1) receptor attenuates gammaherpesvirus-driven B cell

28 or necrosis factor (TNF)- and interleukin-1 (IL-1) receptor-dependent activation of stellate cells an

29 ons to prevent autoimmune and interleukin-1 (IL-1) receptor-dependent, caspase-1-independent inflamma

30 am of Toll-like receptors and interleukin-1 (IL-1) receptors.

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

32 Interleukin-1 (IL-1) signaling is important for multiple potentially pa

33 are associated with increased interleukin-1 (IL-1) signaling within the central nervous system and ar

34 Genetic deletion of interleukin-1 (IL-1) using IL-1alphabeta knockout (KO) mice and periope

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

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

37 ant target classes, including interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-alpha), IL-6, IL

38 centers that operate to drive interleukin-1 (IL-1)-dependent inflammation.

39 nfected macrophages induce an interleukin-1 (IL-1)-dependent inflammatory cytokine response by recrui

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

41 Although microglia did not express IL-1R1, IL-1 stimulation of endothelial cells led to the inducti

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

43 rmal differentiation and activation of IL-31/IL-1 signaling.

44 The mRNA expression levels of IL-6, IL-1 beta, and iNOS were significantly increased in the

45 rs, including C-reactive protein, MX1, IL-6, IL-1, IL-8, TNFalpha, and NF-kappaB.

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

47 ese results validate PAS-IL-1Ra as an active IL-1 antagonist with marked in vivo potency and a signif

48 framework for heme-binding proteins and add IL-1 cytokines to the group of potentially heme-regulate

49 Systemically administered IL-1 receptor antagonist (IL-1RA) was protective against

50 IL-33, an IL-1 family cytokine, is constitutively expressed in muc

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

52 re mediated in part through IL-1, because an IL-1 receptor type 1 antagonist ameliorated the effects

53 uced emergency hematopoiesis and identify an IL-1/MyD88/G-CSF-dependent pathway as the key regulator

54 erimental autoimmune encephalomyelitis in an IL-1 receptor-dependent manner.

55 ubsequently respond to skin commensals in an IL-1-, IL-18-, and antigen-dependent manner.

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

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

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

59 IL-33 is an IL-1 family cytokine that signals through its cognate re

60 IL-33 is an IL-1 family member protein that is a potent driver of in

61 Anakinra, IL-1 receptor antagonist, limited metastasis, and MDSC r

62 ablation or selective expression of IL-1 and IL-1 receptor (IL-1R) in either microglia or endothelia

63 ecific B cells, plasmablasts, and IL-10- and IL-1 receptor antagonist (IL-1RA)-producing Breg cells w

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

65 on of the decoy receptor IL-1 receptor 2 and IL-1 receptor antagonist protein (IL1Ra).

66 For example, in asthma, both IL-33 and IL-1 are of major importance, as are IL-36 and IL-1 in p

67 -1 are of major importance, as are IL-36 and IL-1 in psoriasis.

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

69 IK-dependent NLRP3 inflammasome assembly and IL-1 synthesis, resulting in autocrine/paracrine IL-1bet

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

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

72 e of monocytes/macrophages, granulocytes and IL-1 signaling was investigated using depletion or block

73 hogenetic role of the NLRP3 inflammasome and IL-1 cytokines in the formation, progression, and compli

74 ing active in acute cardiac inflammation and IL-1 in the subsequent development of coronary vasculiti

75 Unlike TNF inhibitors and IL-1 inhibitors, established drugs such as glucocorticoi

76 Monocytes/macrophages and IL-1 signaling were required to protect trained mice fro

77 be necessary to integrate other metals, and IL-1 into the Fe-miR-346 activity network.

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

79 activation of a MyD88-dependent pathway and IL-1 receptor signaling, control of viral replication by

80 e and epidermal differentiation pathways and IL-1 family members (i.e. IL36RN) but not elements of th

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

82 d genital CD4+ T-cell HIV susceptibility and IL-1 levels, but dramatically increased the genital chem

83 Thus, TNF and IL-1 appear to play temporally distinct roles in KD, wit

84 been a major research goal, and both TNF and IL-1 have been identified as potential candidates.

85 ammation: two specific receptor antagonists (IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor ant

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

87 e trans-disease therapeutic activity of anti-IL-1 strategies argues for immunity and inflammation as

88 in, uncovering the potential benefit of anti-IL-1 therapies for pain management in patients with chro

89 uld represent relevant adjuvants to the anti-IL-1 drugs in patients with CAPS and other IL-1-driven d

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

91 hich release potent immune cytokines such as IL-1 and IL-18, contribute to various diseases.

92 ng to local production of cytokines, such as IL-1, by resident islet leukocytes.

93 proinflammatory and proatherogenic (such as IL-1, IL-6, and TNF [tumor necrosis factor]) or as anti-

94 0.01, r = -0.250, respectively), as well as IL-1 receptor antagonist (P < 0.01, r = -0.232 at the be

95 We also review the clinically available IL-1 inhibitors, although not currently approved for car

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

97 the source of IL-1 and the mechanisms behind IL-1 release remain unclear.

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

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

100 kinra, to prevent or treat CRPS via blocking IL-1 actions.

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

102 Similar mechanisms are activated by IL-1.

103 This process is driven by IL-1/MyD88-dependent production of G-CSF.

104 +) cells and its expression was increased by IL-1 and LPS.

105 e central nervous system and are mediated by IL-1 receptor 1 (IL-1R1) on several distinct cell types.

106 ut not prevented in IL-1RI(-/-) mice, nor by IL-1 receptor antagonist (IL-1RA; 10 mg/kg).

107 ytokine pathways with upstream regulation by IL-1 and TNF in adiponectin-deficient mice with decrease

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

109 as danger signals released from dead cells, IL-1 family cytokines can be secreted in the absence of

110 the IL-33 receptor (ST2) and its coreceptor, IL-1 receptor accessory protein, into a single fusion pr

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

112 l circuitry with inhibitors of the cytokines IL-1 and TNF-alpha attenuated myelopoiesis in old mice.

113 volvement in the production of the cytokines IL-1 and/or IL-18.

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

115 ng brain and that these occur by dissociable IL-1-dependent processes.

116 itis, and no clinical trials blocking either IL-1 have yet to be performed.

117 In this Review, each of the eleven IL-1 family cytokines and their receptors are discussed,

118 of the IL-33 receptor gene Il1rl1 (encoding IL-1 receptor-like 1, also known as ST2) in ILC2p and co

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

120 efv(M680I/M680I) FMF knock-in mice exhibited IL-1-dependent increased survival relative to wild-type

121 to track and reciprocally delete or express IL-1 receptor 1 (IL-1R1) in specific cell types, includi

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

123 a)) and other Th cells, and are enriched for IL-1 and NF-kappaB gene signatures.

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

125 RC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth.

126 opts an innate immune pathway resulting from IL-1 stimulation of neurons to induce reactivation.

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

128 Furthermore, IL-1 is known to stimulate beta-cell expression of iNOS

129 us-encoded conserved protein kinase and host IL-1 signaling promote irrelevant B cell responses and g

130 How IL-1 directs these cells to produce inflammatory cytokin

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

132 Critically, although mice deficient in IL-1 signaling have extensive acute inflammation followi

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

134 e reflected in nasal epithelium and included IL-1 receptor like 1, prostaglandin-endoperoxide synthas

135 ammatory cytokines and chemokines, including IL-1, TNF-alpha, IL-9, CXCL1, CCL2, and CCL5 in the bron

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

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

138 d protein kinase-dependent Ripk1-independent IL-1 and tumor necrosis factor production, and were pron

139 ession of epidermal barrier proteins, induce IL-1 signaling, and recruit cells involved in skin infla

140 -3085-3p functions in chondrocytes to induce IL-1-signaling, reduce TGFbeta1 signaling, and inhibit e

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

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

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

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

145 (Ptpn6(DeltaPMN)) is sufficient to initiate IL-1 receptor-dependent cutaneous inflammatory disease,

146 are recently described members of the larger IL-1 cytokine family known to exert potent inflammatory

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

148 cluding NF-kB signaling, IL-6 signaling, LPS/IL-1-mediated inhibition of RXR Function, PI3K in B lymp

149 se mice showed significant increases in lung IL-1 beta mRNA expression, but not the protein, compared

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

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

152 3 impairs cognition by activating microglial IL-1 receptor 1 (IL-1R1).

153 te more IL-1alpha and less IL-1RA, a natural IL-1 receptor antagonist.

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

155 part recovered by blocking TNF-alpha but not IL-1.

156 Naturally-occurring IL-1 receptor antagonist (IL-1Ra) binds and blocks the I

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

158 Ex vivo, the addition of IL-1 receptor antagonist anakinra to whole blood reduced

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

160 eta, IL-18, and IL-1alpha but low amounts of IL-1 receptor antagonist.

161 ne efficacy and safety of the association of IL-1 receptor antagonist anakinra plus methylprednisolon

162 ntly, there has been a strong association of IL-1 with PTB.

163 Despite the development of IL-1 blocking agents, therapeutic blockade of select IL-

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

165 Targeted ablation or selective expression of IL-1 and IL-1 receptor (IL-1R) in either microglia or en

166 Here, we review the complex functions of IL-1 family members in the orchestration of innate and a

167 Here we examined the impact of IL-1 signaling, a key regulator of the IL-17 pathway, in

168 of endothelial cells led to the induction of IL-1 in microglia.

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

170 riptional analyses identified lower level of IL-1 receptor-like 1 (ST2) expression in microglia/macro

171 Cases had higher levels of IL-1 receptor antagonist (IL-1Ra) at all time points lea

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

173 morphologic changes, increased production of IL-1, and enhanced proliferation without triggering leuk

174 Transcriptome profiling of IL-1 receptor (IL-1R)-depleted senescent cells indicates

175 leviated human monocyte-dependent release of IL-1 and IL-6 in a xenotransplanted B-cell lymphoma mode

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

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

178 We discuss the varied roles of IL-1 family members in immune homeostasis and their cont

179 m (CNS), but the cell-type-specific roles of IL-1 signaling are unclear.

180 The pro-tumorigenic roles of IL-1 were counteracted by its effects on myeloid cells,

181 In many cases, secretion of IL-1 cytokines appears to be closely coupled to cell dea

182 eous inflammatory disease, but the source of IL-1 and the mechanisms behind IL-1 release remain uncle

183 ction with PHB1 and OPA1 upon stimulation of IL-1.

184 We propose that models used in the study of IL-1 release should be considered context-dependently.

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

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

187 cachexia as a cost of long-term reliance on IL-1-mediated tolerance mechanisms.

188 eutralizing antibody, recombinant IL-1RA, or IL-1 receptor-targeting small interfering RNA suppresses

189 A xanthine oxidase inhibitor or IL-1 receptor antagonist was administered during RSV inf

190 on receptors, such as Toll-like receptors or IL-1 family receptors.

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

192 i-IL-1 drugs in patients with CAPS and other IL-1-driven diseases.

193 ate, including inflammasomopathies and other IL-1-related conditions, interferonopathies, and disorde

194 ardiovascular indications, and discuss other IL-1 inhibitors, not currently approved, as well as oral

195 phabeta knockout (KO) mice and perioperative IL-1 receptor type 1 (IL-1R1) blockade with the drug ana

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

197 IL-36 cytokines are proinflammatory IL-1 superfamily members, yet their role in enteropathog

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

199 t were recruited to the brain and propagated IL-1-mediated inflammation and anxiety.

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

201 1 and high expression of the decoy receptor IL-1 receptor 2 and IL-1 receptor antagonist protein (IL

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

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

204 ow promising data with anakinra, recombinant IL-1 receptor antagonist, in patients with ST-segment-el

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

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

207 cking agents, therapeutic blockade of select IL-1 family members for periodontitis has only been part

208 Rilonacept, a soluble IL-1 receptor chimeric fusion protein neutralizing IL-1a

209 Specific IL-1 family cytokines are expressed by cells as cytosoli

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

211 Pro-inflammatory cytokines, specifically IL-1 and TNF-alpha, induce aberrant expression of catabo

212 sk of MI, supporting the rationale to target IL-1 activation to reduce cardiovascular risk in PWH.

213 letion in hippocampal neurons confirmed that IL-1 receptor in the hippocampus was critical for stress

214 We hypothesize that IL-1 acts on this subset of hippocampal neurons to influ

215 -1R)-depleted senescent cells indicates that IL-1 controls the late arm of the senescence secretome,

216 n either microglia or endothelia reveal that IL-1-dependent signaling between these cells mediates mi

217 ed transgenic mouse technology, we show that IL-1-dependent microglia-endothelia cross talk is necess

218 We recently showed that IL-1-induced glycolytic reprogramming contributes to all

219 The IL-1 and NLRP3 inflammasome pathways are markedly less r

220 The IL-1 cytokines are considered among the first family of

221 The IL-1 family also contains four members that suppress inf

222 The IL-1 family member IL-37 broadly suppresses innate infla

223 The IL-1 receptor antagonist (IL-1Ra) has emerged as a pivot

224 The IL-1 signaling pathway has been shown to play a critical

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

226 dence linking the NLRP3 inflammasome and the IL-1 cytokines with the pathogenesis of cardiovascular d

227 ely include targeted inhibitors to block the IL-1 isoforms, and possibly oral NLRP3 inflammasome inhi

228 tor antagonist (IL-1Ra) binds and blocks the IL-1 receptor-1 (IL-1R1), preventing signaling.

229 targets, including cytokine signaling by the IL-1 receptor (IL-1R) pathway and inflammasome activatio

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

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

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

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

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

235 a potential role for the inflammasome in the IL-1-mediated innate response to infection.

236 -1R2 deficiency on neutrophils increased the IL-1-induced response of fibroblasts in trans.

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 However, the role of the IL-1 axis in T. gondii infection is unclear.

240 Rationale: IL-18 is a member of the IL-1 cytokine family, and elevated blood IL-18 concentra

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

242 g pathways that involve six cytokines of the IL-1 family (IL-1alpha, IL-1beta, IL-33, IL-36alpha, IL-

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

244 other cytokine family, the 11 members of the IL-1 family are associated with innate immune responses,

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

246 Here, we review the key properties of the IL-1 family members and provide insights into targeting

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

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

249 IL-1beta is the most studied of the IL-1 family of cytokines, including 11 members, among wh

250 Interleukin-37 (IL-37), a member of the IL-1 family of cytokines, is a fundamental suppressor of

251 In addition, levels of the IL-1 family of inflammatory cytokines, as well as the ne

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

253 ulate inflammation, with the majority of the IL-1 family proteins being secreted from immune cells vi

254 ytokines are pro-inflammatory members of the IL-1 family that are upregulated in inflammatory disorde

255 -18 and IL-1beta, which are cytokines of the IL-1 family, are synthesized as precursor proteins and a

256 Compared with other members of the IL-1 family, both the N and the C termini of IL-37 are e

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

258 dentified important roles for members of the IL-1 family-IL-18, IL-33, IL-36, IL-37, and IL-38-in inf

259 mmatory and anti-inflammatory members of the IL-1 family.

260 th IL-1beta and IL-1alpha are members of the IL-1 family; however, their distinct roles in the inflam

261 Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tu

262 Ex vivo, addition of the IL-1 receptor antagonist anakinra to whole blood reduced

263 We conclude that early blockade of the IL-1 receptor is therapeutic in acute hyperinflammatory

264 3s, acetate-FFAR2 augments expression of the IL-1 receptor, which boosts IL-22 secretion in response

265 IL-38 is the most recent member of the IL-1 superfamily and has anti-inflammatory properties si

266 the three best-characterized members of the IL-1 superfamily, IL-1alpha, IL-1beta, and IL-18, in a r

267 hlighting the protumorigenic property of the IL-1-dependent SASP in this context.

268 Loss of alpha-toxin or the IL-1 receptor increases Treg enrichment, whereas topical

269 inhibitors of the NLRP3 inflammasome or the IL-1 receptor-targeting biological agent anakinra.

270 o the therapeutic potential of targeting the IL-1 pathway in inflammatory cancers.

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

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

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

274 ID-19 patients early in the disease with the IL-1 receptor antagonist, anakinra.

275 Over the years, the IL-1 family expanded to include 11 members of cytokines,

276 Therapeutic IL-1-receptor blockade or NLRP3-inhibition reduces myelo

277 ion that increases EC immunogenicity through IL-1 receptor signaling.

278 nduced signals were mediated in part through IL-1, because an IL-1 receptor type 1 antagonist amelior

279 Thus, IL-1 signaling elicits cell-type-specific responses, whi

280 (IRAK1), a key signaling mediator in the TLR/IL-1 pathway, plays a critical role in PTB.

281 contrast to this early involvement for TNF, IL-1 signaling is dispensable for the development of acu

282 mulation of IL-1alpha or IL-1beta binding to IL-1 receptor showed distinct interaction sites that cor

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

284 ed the assembly of inflammasomes, leading to IL-1 family cytokine release from living (hyperactive) o

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

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

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

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

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

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

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

292 ave been completed or are underway utilizing IL-1, IL-23, IL-17, complement, and Jak inhibition, alth

293 at visceral adipose NLRP3 impairs memory via IL-1-mediated microglial activation and suggest that NLR

294 antibody specifically inhibits signaling via IL-1, IL-33 and IL-36 in vitro.

295 ents, and LTP impairment in TRANSWT mice was IL-1 dependent.

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

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

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

299 ter activity in HEK293 cells stimulated with IL-1 and TNF-alpha.

300 Selected mice were treated with IL-1 receptor antagonist (IL-1RA), anti-IL-1beta, or rec