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1 ream of multiple Toll-like receptors and the interleukin-1 receptor.
2 ner dependent on signaling downstream of the interleukin-1 receptor.
3 s the key signaling adapter of Toll-like and interleukin-1 receptors.
6 In the amygdala significant up-regulation of interleukin-1 receptor 1 (IL1r1), interleukin-4 receptor
7 The 28-kDa form of IL-1beta cannot activate interleukin-1 receptor-1 (IL1R1) to signal inflammatory
8 terleukin-6) and alloimmune activation (CD3, interleukin-1 receptor 2, programmed cell death-1, and s
9 rferon-gamma, interleukin-6) and alloimmune (interleukin-1 receptor 2, programmed cell death-1, and s
10 013) describe a molecular system implicating interleukin-1 receptor-2 (IL-1R2) as a principal cytosol
11 to caspase proteolytic activity that cleaves interleukin-1 receptor-2, allowing IL-1alpha dissociatio
12 n assays show that IL-1alpha associates with interleukin-1 receptor-2, and this association is decrea
13 in 1 pathway, through either ablation of the interleukin 1 receptor 8 (IL-1R8, also known as SIGIRR o
15 elated (SIGIRR), which is also known as Toll/interleukin-1 receptor 8 (TIR-8), is a member of the TIR
16 rinsic to B cells and was independent of the interleukin-1 receptor, a cytokine receptor that also si
20 the X-linked intellectual disability protein interleukin-1 receptor accessory protein like 1 (IL1RAPL
21 E) epsilon4 status was identified in IL1RAP (interleukin-1 receptor accessory protein; rs12053868-G;
23 ndings broaden our understanding of how Toll/interleukin-1 receptor adaptor proteins may participate
25 t of T2D, including the inflammation markers interleukin-1 receptor agonist (IL-1RA) and high-sensiti
27 h rituximab alone, increased serum IL-12 and interleukin 1 receptor antagonist (IL-1RA) (P = .005 and
29 centrations of interleukin 1beta (IL-1beta), interleukin 1 receptor antagonist (IL-1Ra), and granuloc
30 lymorphisms of interleukin 1 beta (IL1B) and interleukin 1 receptor antagonist (IL1RA) genes for asso
31 rogation of the MSC transcriptome identified interleukin 1 receptor antagonist (IL1RN) as a potential
33 d P = .00005 for IMI, by the log-rank test), interleukin 1 receptor antagonist (IL1RN; rs419598; P =
35 nduced protein [IP-10]) and proinflammatory (interleukin 1 receptor antagonist [IL-1RA], IL-6) cytoki
36 sis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating
37 itric oxide synthase, interleukin-1beta, and interleukin 1 receptor antagonist but not transforming g
38 roglial numbers, increased interleukin 6 and interleukin 1 receptor antagonist messenger RNA, alterat
40 lts showed a significant increase in IL-1RA (interleukin 1 receptor antagonist) mRNA expression and a
41 ectrin breakdown product 150, interleukin 6, interleukin 1 receptor antagonist, and c-reactive protei
42 tory factor/glycosylation-inhibiting factor, interleukin 1 receptor antagonist, and serine protease i
43 in 6, granulocyte colony-stimulating factor, interleukin 1 receptor antagonist, and vascular endothel
46 the impact of an exogenous recombinant human interleukin-1 receptor antagonist (anakinra) in experime
47 multifocal osteomyelitis, deficiency of the interleukin-1 receptor antagonist (DIRA), Majeed syndrom
48 10 kDa (IP-10) (53-fold) and an increase in interleukin-1 receptor antagonist (IL-1ra) (5-fold) were
49 lute partial correlation coefficients >0.40: Interleukin-1 receptor antagonist (IL-1Ra) and IL-8.
50 f the folded and unfolded ensembles of human interleukin-1 receptor antagonist (IL-1ra) are strongly
51 ty of the method was demonstrated with human interleukin-1 receptor antagonist (IL-1ra) as a protein
53 L-1beta and its regulation by the endogenous interleukin-1 receptor antagonist (IL-1ra) in glutamate
55 e investigated whether the anti-inflammatory interleukin-1 receptor antagonist (IL-1Ra) prevents muri
56 itors enhance the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1Ra) secretion in
57 production of the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1RA) that could be
58 and structural behavior of human recombinant interleukin-1 receptor antagonist (IL-1ra) was revealed
61 necrosis factor (TNF) receptor-2 (TNFR2) and interleukin-1 receptor antagonist (IL-1ra) were fused to
64 culating levels of C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), and soluble
65 6), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 receptor antagonist (IL-1RA), and transfor
66 so occurred, with GVHD-specific secretion of interleukin-1 receptor antagonist (IL-1Ra), IL-18, and C
67 single IFN target gene, Il1rn, which encodes interleukin-1 receptor antagonist (IL-1Ra), is sufficien
70 at a single intracisternal administration of interleukin-1 receptor antagonist (IL-1RA; 112 mug) at t
71 sma levels of neopterin (P<;0.0001), soluble interleukin-1 receptor antagonist (P<;0.0001), IL-8 (P=0
72 nd methionine oxidation in recombinant human interleukin-1 receptor antagonist (rhIL-1ra) was investi
73 interleukin-10 (IL-10), and increased plasma interleukin-1 receptor antagonist (sIL-1ra) and soluble
74 6], tumor necrosis factor-alpha [TNF-alpha], interleukin-1 receptor antagonist [IL-1RA], and transfor
75 D and confirmed six proteins (leptin, renin, interleukin-1 receptor antagonist [IL-1ra], hepatocyte g
76 ate immune system and chemotactic signaling (interleukin-1 receptor antagonist [IL-1Ra], IL-6, IL-8,
77 that can be blocked by administration of an interleukin-1 receptor antagonist and a specific p38 MAP
79 3), and antiinflammatory markers (increased interleukin-1 receptor antagonist and lower monocyte and
80 py efficacy stemmed from the upregulation of interleukin-1 receptor antagonist and suppression of MDS
82 rosis factor-alpha and interleukin-6 and the interleukin-1 receptor antagonist compared with control
84 ombinant activated protein C, talactoferrin, interleukin-1 receptor antagonist in sepsis, and muscle
85 ntagonist gene overexpression has shown that interleukin-1 receptor antagonist is cardioprotective du
86 ral infiltrates are associated with elevated interleukin-1 receptor antagonist or interleukin-8 and 2
87 l activation by minocycline or by transgenic interleukin-1 receptor antagonist overexpression rescued
88 in plasma interleukin-8, interleukin-10, and interleukin-1 receptor antagonist posttransfusion compar
91 akinra is a recombinant version of the human interleukin-1 receptor antagonist used to treat autoinfl
92 ling for age, gender, and primary diagnosis, interleukin-1 receptor antagonist was higher on study da
93 nd 2, C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist were measured in 233 i
94 or necrosis factor-alpha, interleukin-6, and interleukin-1 receptor antagonist), their mRNA expressio
96 associated with augmented concentrations of interleukin-1 receptor antagonist, a key anti-inflammato
97 alpha2beta1 integrin polyclonal antibodies, interleukin-1 receptor antagonist, and the chemical inhi
98 interleukin-1 antibody, or anakinra, a human interleukin-1 receptor antagonist, improved beta-cell fu
100 We investigated the effects of anakinra, an interleukin-1 receptor antagonist, on coronary and left
102 ed growth factor receptors, and anakinra, an interleukin-1 receptor antagonist, respectively, increas
107 We hypothesized that administration of IL-1 (interleukin-1) receptor antagonist (anakinra) could inhi
110 to empirical treatment with the recombinant interleukin-1-receptor antagonist anakinra in the first
112 sed by mutations of IL1RN, which encodes the interleukin-1-receptor antagonist, with prominent involv
113 regulation of 2 inhibitors of TLR signaling: Interleukin 1 Receptor Associated Kinase (IRAK) M, and S
114 differentiation primary response 88 (MYD88)/interleukin-1 receptor associated kinase (IRAK) pathway,
116 gh tyrosine nitration-mediated impairment of interleukin-1 receptor associated kinase (IRAK)4, a sign
117 a series of pyrrolopyrimidine inhibitors of interleukin-1 receptor associated kinase 4 (IRAK4) using
118 s undertaken to test the candidacy of IRAK1 (interleukin-1 receptor associated kinase-1) as an X chro
119 canonical downstream signaling intermediates interleukin 1 receptor-associated kinase (IRAK) and Ikap
121 mammals and overlaps with the 5' UTR of the interleukin 1 receptor-associated kinase (IRAK1) gene.
122 of EGFR and the NF-kappaB regulatory kinase interleukin 1 receptor-associated kinase 1 (IRAK-1).
126 e residues in the known TLR pathway kinases, Interleukin-1 receptor-associated kinase (IRAK) 2 and IR
127 pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex.
129 nes encoding non-RD kinases belonging to the interleukin-1 receptor-associated kinase (IRAK) family.
130 pretreatment in vivo inhibited expression of interleukin-1 receptor-associated kinase (IRAK)-1 while
132 s study, we examined the contribution of the interleukin-1 receptor-associated kinase 1 (IRAK-1) to L
133 id differentiation primary response (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK-1), and
134 ion with NF-kappaB-inducing kinase (NIK) and interleukin-1 receptor-associated kinase 1 (IRAK-1), deg
137 use of TMP with Bruton's tyrosine kinase or interleukin-1 receptor-associated kinase 1 and 4 inhibit
139 ed NFkappaB activation, via interaction with interleukin-1 receptor-associated kinase 2 (IRAK2).
140 B cells isolated from patients deficient for interleukin-1 receptor-associated kinase 4 (IRAK-4), mye
141 onse was reversed in the patient, but not in interleukin-1 receptor-associated kinase 4 (IRAK-4)-defi
145 ying very rare loss-of-function mutations in interleukin-1 receptor-associated kinase 4 (IRAK4), a cr
148 he Toll-like receptor (TLR) pathway, such as interleukin-1 receptor-associated kinase 4 deficiency, h
149 R4-mediated signaling pathway (reduced MyD88-interleukin-1 receptor-associated kinase [IRAK] interact
150 Abs induced activation of TLR4 and triggered interleukin-1 receptor-associated kinase phosphorylation
151 main containing adaptor protein)-MyD88-IRAK (interleukin-1 receptor-associated kinase)1/4-TRAF6 (TNF
153 o-1 actions were likely to be independent of interleukin-1 receptor-associated kinase-1 (IRAK-1) regu
154 miRNA-146a down-regulates expression of the interleukin-1 receptor-associated kinase-1 (IRAK-1), an
155 h diminished IL-1beta-induced degradation of interleukin-1 receptor-associated kinase-1 (IRAK-1).
156 gulating Lys-63-linked polyubiquitination of interleukin-1 receptor-associated kinase-1 (IRAK1) by th
157 pression, myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, and nuclear
159 Within innate immune signaling pathways, interleukin-1 receptor-associated kinases (IRAKs) fulfil
160 its DD and TIR domain and interacts with the interleukin-1 receptor-associated kinases (IRAKs) to for
161 A possible involvement of the gene IL1RAP (interleukin-1 receptor-associated protein) in the pathog
164 entricular assist device, treatment with the interleukin-1 receptor blocking agent anakinra 100 mg/d
166 arized macrophages that highly expresses the interleukin-1 receptor, CD206 and interleukin-4 receptor
169 le nucleotide polymorphism A471T in the Toll-interleukin 1 receptor domain (TIR) of the IL-1Rrp2 that
170 ctivate downstream signaling via TIRAP (Toll-interleukin 1 receptor domain containing adaptor protein
172 ne spanning region and an intracellular Toll/Interleukin 1 receptor domain which invokes signal trans
173 d differentiation factor 88 (MyD88) and toll/interleukin 1 receptor domain-containing adapter inducin
174 d differentiation factor 88 (MyD88) and Toll-interleukin 1 receptor domain-containing adapter inducin
175 8-independent TLR signals by inhibiting Toll/interleukin 1 receptor domain-containing adaptor inducin
176 rimary response protein 88 (MyD88), and Toll interleukin 1 receptor domain-containing adaptor protein
177 with mice lacking signaling through the Toll-Interleukin 1 Receptor Domain-Containing Adaptor Protein
178 ndicating that the Toll-6 receptor, the Toll/interleukin-1 receptor domain adaptor dSARM, and FoxO fu
179 Pharmacologic and genetic disruption of Toll/interleukin-1 receptor domain-containing adapter inducin
181 d differentiating factor 88 (MyD88) and Toll/interleukin-1 receptor domain-containing adapter-inducin
182 cell line Mono Mac 6, induction of the Toll-interleukin-1 receptor domain-containing adaptor-inducin
183 duced autophagy was regulated through a Toll-interleukin-1 receptor domain-containing adaptor-inducin
184 production of ETs by S cells requires a Toll/Interleukin-1 receptor domain-containing protein TirA an
186 e deficient in the TLR adaptor proteins Toll/interleukin-1 receptor-domain-containing adaptor protein
188 r the SAM (sterile alpha motif) or TIR (Toll-interleukin-1 receptor) domains abolishes the ability of
189 the patient-specific characteristics of the interleukin-1 receptor family member ST2 in patients wit
190 s to examine the value of measurement of the interleukin-1 receptor family member ST2 in patients wit
191 Four biomarkers, soluble form of ST2 (an interleukin-1 receptor family member), galectin-3, matri
194 chemoattractant protein-1, resistin, soluble interleukin-1 receptor I, soluble interleukin-2 receptor
196 activation is mediated through TRAF6 in the interleukin 1 receptor (IL-1R) and toll-like receptor (T
197 h their role in Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) mediated signaling pathwa
198 LLIP) regulates Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) signaling against mycobac
199 ive influenza A virus, signaling through the interleukin 1 receptor (IL-1R) was required for producti
200 DA-5), as well as cytokine receptors such as interleukin 1 receptor (IL-1R), have been implicated in
201 ated innate signaling pathway, as well as in interleukin-1 receptor (IL-1R) and IL-18R signaling.
203 d was first characterized as an inhibitor of interleukin-1 receptor (IL-1R) and Toll-like receptor (T
204 on of IRAK1, a kinase thus far implicated in interleukin-1 receptor (IL-1R) and Toll-like receptor (T
205 nown that TLR3 uses the adaptor protein Toll/interleukin-1 receptor (IL-1R) domain-containing adaptor
206 members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signal
207 ta (IkappaBzeta), a Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) inducible transcription f
208 We found that Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) signaling dynamics relied
209 ), a negative regulator of the Toll-like and interleukin-1 receptor (IL-1R) signaling pathways, contr
211 e expression of the Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily, IL-1beta pro
213 ting microglia expressed high amounts of the interleukin-1 receptor (IL-1R), and treatment with an IL
214 a signaling adaptor shared by most TLRs and interleukin-1 receptor (IL-1R), in an in vitro model of
215 c expression of toll-like receptor 4 (TLR4), interleukin-1 receptor (IL-1R), or interferon-gamma rece
218 inhibitors to assess the regulatory roles of interleukin-1 receptor (IL-1R)-associated kinase 4 (IRAK
219 fied nearly two decades ago as a mediator of interleukin-1 receptor (IL-1R)-mediated activation of NF
220 ponses are controlled through members of the interleukin-1 receptor (IL-1R)/Toll-like receptor superf
223 in that links toll-like receptors (TLRs) and Interleukin-1 receptors (IL-1Rs) with downstream signali
225 D88(-/-), MyD88/TLR adaptor molecule 1(-/-), interleukin-1 receptor [IL-1R1](-/-), and interleukin (I
227 d deficiencies in the inflammatory response, interleukin-1 receptor knockout (IL-1R(-/-)) and caspase
228 -/-)), caspase-1 knockout (Casp-1(-/-)), and interleukin-1 receptor knockout (IL-1R(-/-)) mice treate
230 ied the expression of IL36 and its receptor, interleukin 1 receptor like 2 (IL1RL2 or IL36R) in the d
231 ivates many immune cell types expressing the interleukin 1 receptor-like 1 (IL1RL1) receptor ST2, inc
234 dipocyte differentiation, whereas Got2, Cpq, interleukin-1 receptor-like 1/ST2-IL-33, Sparc, and Lgal
235 mune receptors containing an N-terminal Toll-interleukin-1 receptor-like domain (TNLs) in Arabidopsis
237 because deletion of Nlrp3, caspase-1 and the interleukin-1 receptor markedly protects against rheumat
239 uide cleavage of transcripts of the Toll and Interleukin-1 receptor-NB-LRR immune receptor N from tob
240 r-triggered immunity conditioned by the Toll Interleukin-1 Receptor-nucleotide binding (NB)-Leu-rich
241 gered immunity specifically mediated by Toll-interleukin-1 receptor-nucleotide binding-leucine-rich r
243 all genes predicted to contain either a Toll/interleukin-1 receptor or nucleotide-binding site domain
245 in their N-terminal domains: these are Toll/interleukin-1 receptor resistance (TIR) domain-containin
246 n primary response 88 adaptors, but not toll/interleukin-1 receptor/resistance [TIR] domain-containin
249 mon adaptor for toll-like receptor (TLR) and Interleukin-1 receptor signaling, are critical for radio
253 ignaling by the toll-like receptor (TLR) and interleukin-1 receptor superfamily requires the adapter
254 ch signal through adaptors containing a Toll-interleukin 1 receptor (TIR) domain, such as MyD88 and T
256 n primary response gene 88 (MyD88)- and Toll-interleukin 1 receptor (TIR) domain-containing adaptor i
258 SENSITIVE 3 (CHS3) encodes an atypical Toll/Interleukin 1 Receptor (TIR)-type NLR protein with an ad
259 fied roles in IFN-I stimulation for the Toll-interleukin-1 receptor (TIR) adaptor Myd88 adaptor-like
260 plementation, and found that C15 in the Toll/interleukin-1 receptor (TIR) domain and L816 in the LRR
261 ve to Nicotiana benthamiana with a Toll-like interleukin-1 receptor (TIR) domain bound to the Xanthom
262 neurodegenerative process(5-8), and its Toll/interleukin-1 receptor (TIR) domain exerts its pro-neuro
266 rly Leu265Pro (L265P), within the MyD88 Toll/interleukin-1 receptor (TIR) domain sustain lymphoma cel
267 e-rich repeat (NLR) protein with a Toll-like interleukin-1 receptor (TIR) domain, which mediates XopQ
269 lipopolysaccharide, this is a delayed, Toll/interleukin-1 receptor (TIR) domain-containing adapter-i
270 ckouts including TLR2, TLR4, MyD88, and Toll-interleukin-1 receptor (TIR) domain-containing adaptor p
271 esponses by targeted degradation of the Toll/interleukin-1 receptor (TIR) domain-containing adaptor p
275 ults in dimerization of their cytosolic Toll/interleukin-1 receptor (TIR) domains and recruitment of
276 oth processes depend on closely related Toll/interleukin-1 receptor (TIR) domains in these proteins,
278 Toll-like receptors (TLRs), cytoplasmic Toll/interleukin-1 receptor (TIR) domains of the receptors un
279 The heterotypic interaction between the Toll/interleukin-1 receptor (TIR) domains of TLRs and adaptor
280 aling adapter protein interactions with Toll/Interleukin-1 Receptor (TIR) domains present in sensory
283 illo motif (SARM) is a highly conserved Toll/interleukin-1 receptor (TIR)-containing adaptor protein
284 structures of MAL revealed a nontypical Toll/interleukin-1 receptor (TIR)-domain fold stabilized by t
285 equires the P loops of each protein and Toll/interleukin-1 receptor (TIR)-domain-mediated heteromeric
288 lays an essential role in Toll-like receptor/interleukin-1 receptor (TLR/IL-1R) -associated NF-kappaB
289 can activate signaling by the Toll-like and interleukin-1 receptors (TLR and IL-1R) to mediate patho
290 signalling (tumour necrosis factor receptor/interleukin-1 receptor, TNFR/IL-1R in mammals) is indisp
291 ch are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members
292 he negative regulation of Toll-like receptor/interleukin-1 receptor-triggered inflammatory cascades a
293 terleukin-1beta interacts with its receptor (interleukin 1 receptor type 1) on hematopoietic stem and
294 was developed to analyze recombinant soluble Interleukin 1 receptor type II (sIL-1R type II) drug sub
295 d the role of toll-like receptors (TLRs) and interleukin-1 receptor type 1 (IL-1R1) in S. marcescens-
296 nization, we show that mice deficient in the interleukin-1 receptor type 1 (Il1r1(-/-)) have reduced
297 y protein (IL1RAP; IL1R3) is a coreceptor of interleukin-1 receptor type 1 and has been found upregul
300 IC associated genes included the innate interleukin 1 receptor, type 1 and the antimicrobial pep