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1 t production of the proinflammatory cytokine interleukin-1.
2 ory cytokines like tumor necrosis factor and interleukin-1.
4 n-glucose deprivation (OGD), reperfusion and interleukin-1 alpha (IL-1alpha) stimulate brain cells to
6 y cytokines, including TNF-alpha, IL-1alpha (Interleukin-1 alpha), RANTES (regulated on activation, n
7 se is driven by the proinflammatory cytokine interleukin-1 and is known to exacerbate resulting injur
8 y the much lower expression of receptors for interleukin-1 and TGFbeta, downstream protumor factors,
9 ession of proinflammatory cytokines (such as interleukin-1 and tumor necrosis factor-alpha) and chemo
10 ide primarily protects mice by repressing an interleukin-1- and 12/15-lipoxygenase-dependent neutroph
11 periodic syndromes respond to treatment with interleukin-1 antagonists, and single case reports of Sc
13 whether canakinumab, a human monoclonal anti-interleukin-1 antibody, or anakinra, a human interleukin
15 endently in human astrocytes by the cytokine interleukin 1 beta (IL1B), and inactivation of Vegfa in
16 patients with high grade hepatic steatosis, Interleukin 1 beta encoding gene with anorexigenic funct
17 data on the association between SNPs in the interleukin 1 beta gene (IL1B) and colorectal cancer (CR
19 uman articular cartilage, LfcinB antagonizes interleukin-1 beta (IL-1beta) and fibroblast growth fact
20 d secretion of the proinflammatory cytokines interleukin-1 beta (IL-1beta) and IL-18, which help cont
21 and clinical evidence reviewed here support interleukin-1 beta (IL-1beta) as both a local vascular a
24 GF), matrix metalloproteinase 9 (MMP-9), and interleukin-1 beta (IL-1beta) salivary biomarkers in the
27 tor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-1 beta (IL-1beta), and monocyte chemo attrac
28 Interferon-gamma (IFN-gamma), TNF-alpha, interleukin-1 beta (IL-1beta), fibroblast growth factor-
30 , including aryl hydrocarbon receptor (Ahr), interleukin-1 beta (Il1b), estrogen receptor alpha (Esr1
31 n to activity levels through enhanced muscle interleukin-1 beta (IL1beta)/IL1 receptor signaling to g
33 e human cytokine proteins (interferon gamma, interleukin-1 beta, and tumor necrosis factor alpha) wer
34 ading depolarization such as upregulation of interleukin-1 beta, inducible nitric oxide synthase and
35 accumulation, and inhibited proinflammatory (interleukin-1 beta, tumor necrosis factor alpha, and F4/
36 e release of tumor necrosis factor-alpha and interleukin-1 beta, which are pro-inflammatory cytokines
38 juvants.In vitro, these compounds induced an interleukin 1-beta (IL-1beta) response in the macrophage
44 ical and experimental evidence suggests that interleukin-1 blockade is effective against myocardial i
52 tly modified interleukins, components of the interleukin-1 family were significantly up-regulated.
53 te immunity (most notably for members of the interleukin-1 family), which depend on the specific infl
54 lammatory mediators include cytokines of the interleukin-1 family, such as IL-1alpha and IL-1beta.
58 cells and by mitigating the cytotoxicity of interleukin 1 (IL-1) and tumor necrosis factor-alpha (TN
59 randomized trial demonstrate that targeting interleukin 1 (IL-1) by topical application of an IL-1 a
65 nt of bacterial clearance, deficiency in the interleukin 1 (IL-1) receptor led to a significant impai
69 N2 gene expression by ELF3 in the context of interleukin 1 (IL-1)-driven inflammatory responses in ch
72 olecule in inflammatory pathways involved in interleukin 1 (IL-1)/IL-18/Toll-like receptor signaling
74 nce suggests that pro-inflammatory cytokines interleukin-1 (IL-1) and IL-18 show an age-dependent reg
77 of various proinflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha, th
79 to optimize combined anti-CD3 treatment plus interleukin-1 (IL-1) blockade to reverse new-onset disea
80 ry cytokines tumor necrosis factor (TNF) and interleukin-1 (IL-1) but not by growth factors platelet-
85 ed the inflammasome, leading to secretion of interleukin-1 (IL-1) family cytokines, pyroptosis, and c
88 ead to caspase activation and release of the interleukin-1 (IL-1) family members, IL-1beta and IL-18.
89 which include Toll-like receptors (TLRs) and interleukin-1 (IL-1) family members, we found that MyD88
96 sion of the pivotal proinflammatory cytokine interleukin-1 (IL-1) is increased in CML bone marrow.
100 Overexpression of several markers such as interleukin-1 (IL-1) receptor accessory protein (IL1RAP)
101 esponding normal cells, express a functional interleukin-1 (IL-1) receptor complex and respond with N
103 g K63-linked polyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog
104 ic brain injury, and to evaluate the role of interleukin-1 (IL-1) signaling as a target for pharmacol
106 s recently been identified as a regulator of interleukin-1 (IL-1) signaling, but its roles in regulat
108 DCs are defined by their ability to release interleukin-1 (IL-1) while maintaining cell viability, e
116 r molecule that mediates the TNFR family and interleukin-1 (IL-1)/Toll-like receptor (TLR) signaling
117 ls), and measured levels of cytokines of the interleukin 1 (IL1) family (IL1alpha, IL1beta, IL1ra, an
118 r toll-like receptors and also implicated in interleukin-1 (Il1) signaling, in a murine model of exte
119 ption of IFNB1 but not of the genes encoding interleukin-1 (IL1), interleukin-6 (IL6), or tumor necro
120 g to a role for the proinflammatory cytokine interleukin-1 in myocardial inflammation and contractile
129 l of the M1-pUb chains formed in response to interleukin-1, or the Toll-Like Receptors 1/2 agonist Pa
130 Here we show that hyperactivation of the interleukin 1 pathway, through either ablation of the in
131 cytokines (such as tumor necrosis factor and interleukin-1), reactive oxygen species (ROS), pathogens
132 activation is mediated through TRAF6 in the interleukin 1 receptor (IL-1R) and toll-like receptor (T
133 h their role in Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) mediated signaling pathwa
134 LLIP) regulates Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) signaling against mycobac
135 ive influenza A virus, signaling through the interleukin 1 receptor (IL-1R) was required for producti
136 DA-5), as well as cytokine receptors such as interleukin 1 receptor (IL-1R), have been implicated in
138 n primary response gene 88 (MyD88)- and Toll-interleukin 1 receptor (TIR) domain-containing adaptor i
140 SENSITIVE 3 (CHS3) encodes an atypical Toll/Interleukin 1 Receptor (TIR)-type NLR protein with an ad
142 in 1 pathway, through either ablation of the interleukin 1 receptor 8 (IL-1R8, also known as SIGIRR o
145 h rituximab alone, increased serum IL-12 and interleukin 1 receptor antagonist (IL-1RA) (P = .005 and
147 centrations of interleukin 1beta (IL-1beta), interleukin 1 receptor antagonist (IL-1Ra), and granuloc
148 lymorphisms of interleukin 1 beta (IL1B) and interleukin 1 receptor antagonist (IL1RA) genes for asso
150 d P = .00005 for IMI, by the log-rank test), interleukin 1 receptor antagonist (IL1RN; rs419598; P =
152 nduced protein [IP-10]) and proinflammatory (interleukin 1 receptor antagonist [IL-1RA], IL-6) cytoki
153 sis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating
154 itric oxide synthase, interleukin-1beta, and interleukin 1 receptor antagonist but not transforming g
155 tory factor/glycosylation-inhibiting factor, interleukin 1 receptor antagonist, and serine protease i
157 le nucleotide polymorphism A471T in the Toll-interleukin 1 receptor domain (TIR) of the IL-1Rrp2 that
158 ctivate downstream signaling via TIRAP (Toll-interleukin 1 receptor domain containing adaptor protein
159 ne spanning region and an intracellular Toll/Interleukin 1 receptor domain which invokes signal trans
160 rimary response protein 88 (MyD88), and Toll interleukin 1 receptor domain-containing adaptor protein
162 mammals and overlaps with the 5' UTR of the interleukin 1 receptor-associated kinase (IRAK1) gene.
165 ivates many immune cell types expressing the interleukin 1 receptor-like 1 (IL1RL1) receptor ST2, inc
167 members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signal
168 ), a negative regulator of the Toll-like and interleukin-1 receptor (IL-1R) signaling pathways, contr
169 e expression of the Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily, IL-1beta pro
171 ting microglia expressed high amounts of the interleukin-1 receptor (IL-1R), and treatment with an IL
172 c expression of toll-like receptor 4 (TLR4), interleukin-1 receptor (IL-1R), or interferon-gamma rece
175 fied nearly two decades ago as a mediator of interleukin-1 receptor (IL-1R)-mediated activation of NF
176 ponses are controlled through members of the interleukin-1 receptor (IL-1R)/Toll-like receptor superf
178 rly Leu265Pro (L265P), within the MyD88 Toll/interleukin-1 receptor (TIR) domain sustain lymphoma cel
179 e-rich repeat (NLR) protein with a Toll-like interleukin-1 receptor (TIR) domain, which mediates XopQ
181 lipopolysaccharide, this is a delayed, Toll/interleukin-1 receptor (TIR) domain-containing adapter-i
182 esponses by targeted degradation of the Toll/interleukin-1 receptor (TIR) domain-containing adaptor p
184 ults in dimerization of their cytosolic Toll/interleukin-1 receptor (TIR) domains and recruitment of
185 Toll-like receptors (TLRs), cytoplasmic Toll/interleukin-1 receptor (TIR) domains of the receptors un
186 aling adapter protein interactions with Toll/Interleukin-1 Receptor (TIR) domains present in sensory
188 structures of MAL revealed a nontypical Toll/interleukin-1 receptor (TIR)-domain fold stabilized by t
189 equires the P loops of each protein and Toll/interleukin-1 receptor (TIR)-domain-mediated heteromeric
190 In the amygdala significant up-regulation of interleukin-1 receptor 1 (IL1r1), interleukin-4 receptor
192 D88(-/-), MyD88/TLR adaptor molecule 1(-/-), interleukin-1 receptor [IL-1R1](-/-), and interleukin (I
195 the X-linked intellectual disability protein interleukin-1 receptor accessory protein like 1 (IL1RAPL
196 E) epsilon4 status was identified in IL1RAP (interleukin-1 receptor accessory protein; rs12053868-G;
197 ndings broaden our understanding of how Toll/interleukin-1 receptor adaptor proteins may participate
200 multifocal osteomyelitis, deficiency of the interleukin-1 receptor antagonist (DIRA), Majeed syndrom
201 lute partial correlation coefficients >0.40: Interleukin-1 receptor antagonist (IL-1Ra) and IL-8.
203 e investigated whether the anti-inflammatory interleukin-1 receptor antagonist (IL-1Ra) prevents muri
204 itors enhance the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1Ra) secretion in
205 production of the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1RA) that could be
207 necrosis factor (TNF) receptor-2 (TNFR2) and interleukin-1 receptor antagonist (IL-1ra) were fused to
209 culating levels of C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), and soluble
211 at a single intracisternal administration of interleukin-1 receptor antagonist (IL-1RA; 112 mug) at t
212 sma levels of neopterin (P<;0.0001), soluble interleukin-1 receptor antagonist (P<;0.0001), IL-8 (P=0
213 D and confirmed six proteins (leptin, renin, interleukin-1 receptor antagonist [IL-1ra], hepatocyte g
215 3), and antiinflammatory markers (increased interleukin-1 receptor antagonist and lower monocyte and
216 py efficacy stemmed from the upregulation of interleukin-1 receptor antagonist and suppression of MDS
217 rosis factor-alpha and interleukin-6 and the interleukin-1 receptor antagonist compared with control
218 l activation by minocycline or by transgenic interleukin-1 receptor antagonist overexpression rescued
219 in plasma interleukin-8, interleukin-10, and interleukin-1 receptor antagonist posttransfusion compar
220 akinra is a recombinant version of the human interleukin-1 receptor antagonist used to treat autoinfl
221 nd 2, C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist were measured in 233 i
222 or necrosis factor-alpha, interleukin-6, and interleukin-1 receptor antagonist), their mRNA expressio
223 associated with augmented concentrations of interleukin-1 receptor antagonist, a key anti-inflammato
224 interleukin-1 antibody, or anakinra, a human interleukin-1 receptor antagonist, improved beta-cell fu
225 We investigated the effects of anakinra, an interleukin-1 receptor antagonist, on coronary and left
227 ed growth factor receptors, and anakinra, an interleukin-1 receptor antagonist, respectively, increas
230 a series of pyrrolopyrimidine inhibitors of interleukin-1 receptor associated kinase 4 (IRAK4) using
233 entricular assist device, treatment with the interleukin-1 receptor blocking agent anakinra 100 mg/d
235 ndicating that the Toll-6 receptor, the Toll/interleukin-1 receptor domain adaptor dSARM, and FoxO fu
236 Pharmacologic and genetic disruption of Toll/interleukin-1 receptor domain-containing adapter inducin
238 cell line Mono Mac 6, induction of the Toll-interleukin-1 receptor domain-containing adaptor-inducin
239 production of ETs by S cells requires a Toll/Interleukin-1 receptor domain-containing protein TirA an
240 Four biomarkers, soluble form of ST2 (an interleukin-1 receptor family member), galectin-3, matri
242 chemoattractant protein-1, resistin, soluble interleukin-1 receptor I, soluble interleukin-2 receptor
243 -/-)), caspase-1 knockout (Casp-1(-/-)), and interleukin-1 receptor knockout (IL-1R(-/-)) mice treate
244 because deletion of Nlrp3, caspase-1 and the interleukin-1 receptor markedly protects against rheumat
245 all genes predicted to contain either a Toll/interleukin-1 receptor or nucleotide-binding site domain
247 mon adaptor for toll-like receptor (TLR) and Interleukin-1 receptor signaling, are critical for radio
250 d the role of toll-like receptors (TLRs) and interleukin-1 receptor type 1 (IL-1R1) in S. marcescens-
251 nization, we show that mice deficient in the interleukin-1 receptor type 1 (Il1r1(-/-)) have reduced
252 y protein (IL1RAP; IL1R3) is a coreceptor of interleukin-1 receptor type 1 and has been found upregul
255 r the SAM (sterile alpha motif) or TIR (Toll-interleukin-1 receptor) domains abolishes the ability of
257 signalling (tumour necrosis factor receptor/interleukin-1 receptor, TNFR/IL-1R in mammals) is indisp
258 The 28-kDa form of IL-1beta cannot activate interleukin-1 receptor-1 (IL1R1) to signal inflammatory
259 013) describe a molecular system implicating interleukin-1 receptor-2 (IL-1R2) as a principal cytosol
260 to caspase proteolytic activity that cleaves interleukin-1 receptor-2, allowing IL-1alpha dissociatio
261 n assays show that IL-1alpha associates with interleukin-1 receptor-2, and this association is decrea
262 pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex.
263 id differentiation primary response (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK-1), and
266 use of TMP with Bruton's tyrosine kinase or interleukin-1 receptor-associated kinase 1 and 4 inhibit
269 ed NFkappaB activation, via interaction with interleukin-1 receptor-associated kinase 2 (IRAK2).
270 onse was reversed in the patient, but not in interleukin-1 receptor-associated kinase 4 (IRAK-4)-defi
272 ying very rare loss-of-function mutations in interleukin-1 receptor-associated kinase 4 (IRAK4), a cr
275 Abs induced activation of TLR4 and triggered interleukin-1 receptor-associated kinase phosphorylation
276 main containing adaptor protein)-MyD88-IRAK (interleukin-1 receptor-associated kinase)1/4-TRAF6 (TNF
277 o-1 actions were likely to be independent of interleukin-1 receptor-associated kinase-1 (IRAK-1) regu
278 Within innate immune signaling pathways, interleukin-1 receptor-associated kinases (IRAKs) fulfil
279 its DD and TIR domain and interacts with the interleukin-1 receptor-associated kinases (IRAKs) to for
280 e deficient in the TLR adaptor proteins Toll/interleukin-1 receptor-domain-containing adaptor protein
281 dipocyte differentiation, whereas Got2, Cpq, interleukin-1 receptor-like 1/ST2-IL-33, Sparc, and Lgal
282 uide cleavage of transcripts of the Toll and Interleukin-1 receptor-NB-LRR immune receptor N from tob
285 We hypothesized that administration of IL-1 (interleukin-1) receptor antagonist (anakinra) could inhi
288 in that links toll-like receptors (TLRs) and Interleukin-1 receptors (IL-1Rs) with downstream signali
296 ture of systemic lupus erythematosus and the interleukin-1 signature in systemic onset juvenile idiop
297 he formation of M1-pUb chains in response to interleukin-1, that the formation of K63-pUb chains is a
298 f clinical response of sJIA and CAPS to anti-interleukin 1 therapies prompted a comparison at the bio
299 kine, that activates multiple members of the interleukin-1/Toll-like receptor (TLR) family associated
300 Fadd and Tnfsf9) and inflammatory (for, eg, interleukin 1, tumor necrosis factor alpha, chemokines,
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