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1 mphocytes) but not in mice deficient for the IL-1 receptor.
2 onal priming effect that was mediated by the IL-1 receptor.
3 a and IL-1beta, both of which signal through IL-1 receptor.
4 diates signaling downstream of the IL-18 and IL-1 receptors.
5 tivated TNF receptors but not with activated IL-1 receptors.
6 am of Toll-like receptors and interleukin-1 (IL-1) receptors.
7 to track and reciprocally delete or express IL-1 receptor 1 (IL-1R1) in specific cell types, includi
8 stinal lamina propria lymphocytes expressing IL-1 receptor 1 (IL-1R1) is the lymphoid tissue inducer
9 e central nervous system and are mediated by IL-1 receptor 1 (IL-1R1) on several distinct cell types.
13 gene expression patterns, we identified the IL-1 receptor 1 (IL1R1) as a direct target of miR-BHRF1-
14 nstrate that a viral miRNA downregulates the IL-1 receptor 1 during EBV infection, which consequently
15 ter hypoxia/reoxygenation was accelerated in IL-1 receptor 1 knockout (IL-1R1 KO) mice, in mice recei
17 ue to their low expression of interleukin 1 (IL-1) receptor 1 and high expression of the decoy recept
19 st cell types examined expressed a cytosolic IL-1 receptor 2 (IL-1R2) whose binding to pro-IL-1alpha
20 1 and high expression of the decoy receptor IL-1 receptor 2 and IL-1 receptor antagonist protein (IL
21 The type 1 IL-1 receptor (IL-1R1) and the IL-1 receptor accessory protein (IL-1RAcP) form a functi
22 in the interleukin 1 (IL-1) cytokine family, IL-1 receptor accessory protein (IL-1RAcP) is the co-rec
23 is: 2 IL33 SNPs (rs4742170 and rs7037276), 1 IL-1 receptor accessory protein (IL1RAP) SNP (rs10513854
24 sregulated expression of 11 genes, including IL-1 receptor accessory protein (IL1RAP), in all leukemi
25 increased expression of the IL-1 receptors, IL-1 receptor accessory protein and IL-1 receptor type 1
26 ch we measured binding to the IL-36 receptor/IL-1 receptor accessory protein complex and functional a
29 the IL-33 receptor (ST2) and its coreceptor, IL-1 receptor accessory protein, into a single fusion pr
30 on of several markers such as interleukin-1 (IL-1) receptor accessory protein (IL1RAP), CD99, T-cell
31 more severe renal epithelial cell damage via IL-1 receptor activation in coculture compared with WT m
32 studied the role of the Toll/interleukin 1 (IL-1) receptor adapter and major inflammatory mediator m
33 A fibrotic infrapatellar fat pad express the IL-1 receptor and on exposure to IL-1alpha polarize to a
34 H2/TH17 cells expressed higher levels of the IL-1 receptor and phospho-p38 mitogen-activated protein
35 Carotid body glomus cells also expressed IL-1 receptor and responded to application of IL-1beta w
37 tokine receptors, but rather, indirectly via IL-1 receptors and TNF receptors being expressed on glia
39 IL-1beta following the severe stressor with IL-1 receptor antagonist (10 mug, intracerebroventricula
41 IL-22 and IL-17 was not that of the classic IL-1 receptor antagonist (anakinra), because low concent
43 y brain-specific overexpression of the human IL-1 receptor antagonist (hIL1ra(Ast)(+/+) mice) leads t
44 ammation: two specific receptor antagonists (IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor ant
45 monocyte production of the natural inhibitor IL-1 receptor antagonist (IL-1Ra) and shifts production
46 IL-1beta, type I IL-1 receptor (IL-1R1), and IL-1 receptor antagonist (IL-1Ra) are all important regu
51 AT1 downregulation, whereas incubation of an IL-1 receptor antagonist (IL-1ra) in EAE slices reduced
54 nction, whereas higher circulating levels of IL-1 receptor antagonist (IL-1RA), an endogenous inhibit
55 pha, of interleukin-1beta (IL-1beta), and of IL-1 receptor antagonist (IL-1ra), and correlated cytoki
57 knockout (IL-1R1 KO) mice, in mice receiving IL-1 receptor antagonist (IL-1RA), and in mice given the
59 2) fragments of anti-CD3 mAb with or without IL-1 receptor antagonist (IL-1RA), or anti-IL-1beta mAb.
60 ecific B cells, plasmablasts, and IL-10- and IL-1 receptor antagonist (IL-1RA)-producing Breg cells w
64 induction of the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1Ra, 16 +/- 1.7 ng/mL, mean
68 evoked inflammatory stress to measure plasma IL-1 receptor antagonist (IL1RA) following low-dose Food
71 0.01, r = -0.250, respectively), as well as IL-1 receptor antagonist (P < 0.01, r = -0.232 at the be
72 luble TNF receptor-1 (sTNFR1; p < .001), and IL-1 receptor antagonist (p value in mania < .001 and eu
73 ased plasma interleukin (IL)-6, IL-1beta and IL-1 receptor antagonist (R=-0.33 to -0.36, P<0.05).
75 mation index ratio of interleukin (IL)-1beta/IL-1 receptor antagonist (ra) using enzyme-linked immuno
76 terleukin [IL]-1 beta [IL-1beta], rs1143623; IL-1 receptor antagonist [IL-1ra], rs4251961; IL-10, rs1
78 breast cancer, we demonstrate here that the IL-1 receptor antagonist anakinra abrogates IL-22 produc
79 neutralization of IL-1 and IL-18, using the IL-1 receptor antagonist anakinra and anti-IL-18 antibod
80 ons in acute-phase hsCRP production with the IL-1 receptor antagonist anakinra and the IL-6 receptor
81 e activation to (1) assess the safety of the IL-1 receptor antagonist anakinra in conjunction with in
82 open-label, single-arm clinical trial of the IL-1 receptor antagonist anakinra in corticosteroid-resi
83 hibitory effect on IL-1beta secretion by the IL-1 receptor antagonist anakinra in phagocytes of patie
84 ne efficacy and safety of the association of IL-1 receptor antagonist anakinra plus methylprednisolon
86 Similarly, intrathecal administration of the IL-1 receptor antagonist anakinra restored locomotor fun
91 nd augmented production of anti-inflammatory IL-1 receptor antagonist and vascular endothelial growth
92 otoxin concentrations correlated with sputum IL-1 receptor antagonist concentrations (r = 0.510, P <
93 RNA against NLRP3, recombinant IL-1beta, and IL-1 receptor antagonist confirmed the role of NLRP3 inf
94 ized that a synonymous coding variant in the IL-1 receptor antagonist gene (IL1RN), rs315952, previou
96 ivated NLRC4 for sustained production of the IL-1 receptor antagonist IL-1Ra, which restrained NLRP3
97 sRNA-dependent production of IL-1, TSLP, and IL-1 receptor antagonist in NHBE cells was regulated by
103 binant human IL-1beta monoclonal antibody or IL-1 receptor antagonist resulted in a dose- and time-de
104 n IL-1beta neutralizing antibody or specific IL-1 receptor antagonist revealed the primary involvemen
106 the human recombinant form of the endogenous IL-1 receptor antagonist used to treat rheumatoid arthri
108 s etanercept (TNFalpha inhibitor), anakinra (IL-1 receptor antagonist), prednisone (NFkappaB transloc
111 inhibitor, or blocking of IL-1 signaling by IL-1 receptor antagonist, abrogated the Th17-promoting e
114 ally benefiting from anakinra, a recombinant IL-1 receptor antagonist, but the utility of other biolo
115 ctively in SL rats and this was prevented by IL-1 receptor antagonist, consistent with a role for IL-
116 ow promising data with anakinra, recombinant IL-1 receptor antagonist, in patients with ST-segment-el
117 with the IL-1 blocker anakinra (recombinant IL-1 receptor antagonist, Kineret(R), Swedish Orphan Bio
119 ved apocynin to inhibit NADPH oxidase (NOX), IL-1 receptor antagonist, or IL-18 binding protein to pr
120 nged with PMN-SA produced more IL-8 and less IL-1 receptor antagonist, TNF-alpha, activated caspase-1
121 expression of IL-1R-associated kinase M and IL-1 receptor antagonist, which are negative regulators
132 n postnatal development and investigated two IL-1 receptor antagonists, the competitive inhibitor ana
135 strated deficient TLR4-induced activation of IL-1 receptor-associated kinase (IRAK) 4, IRAK1, and TAN
136 f various innate immune receptors results in IL-1 receptor-associated kinase (IRAK)-1/IRAK-4-mediated
137 is and depends on the TLR-signaling molecule IL-1 receptor-associated kinase (IRAK-1) and its kinase
138 a greatly up-regulated the protein levels of IL-1 receptor-associated kinase (IRAK-1) and tumor-necro
139 guanine nucleotide exchange factor VAV-1 and IL-1 receptor-associated kinase 1 (IRAK-1), respectively
140 at Tbeta4 treatment suppressed expression of IL-1 receptor-associated kinase 1 (IRAK1) and tumor necr
141 S100A7, S100A8, and S100A9 (S100A7/8/9), and IL-1 receptor-associated kinase 1 (IRAK1) establish a re
142 ike receptor (TLR4) signaling first mediates IL-1 receptor-associated kinase 1 (IRAK1) nuclear transl
143 roduction via binding to and phosphorylating IL-1 receptor-associated kinase 1 (IRAK1), leading to IR
144 R-146a diminished or enhanced, respectively, IL-1 receptor-associated kinase 1 expression and induced
145 actor 7 gene expression and rapidly degraded IL-1 receptor-associated kinase 1 expression in plasmacy
146 adaptor protein (TIRAP), and the downstream IL-1 receptor-associated kinase 1, IL-1 receptor-associa
147 ession of IL-25 and IL-33 by upregulation of IL-1 receptor-associated kinase 1, transforming growth f
149 t domain adaptor inducing IFN-beta (CARDIF), IL-1 receptor-associated kinase 4 (IRAK4), IkappaB kinas
150 he TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor-associated kinase 4 [IRAK-4], TLR3, UNC-93
151 ownstream IL-1 receptor-associated kinase 1, IL-1 receptor-associated kinase 4, and TNF receptor-asso
153 nhibitor of NF-kappaB activation 3 (ABIN-3), IL-1 receptor-associated kinase M (IRAK-M), suppressor o
154 characterize an X chromosome-linked IRAK-1 (IL-1 receptor-associated kinase) polymorphism as an alte
156 mune components such as Toll-like receptors, IL-1 receptor-associated kinase/tumor necrosis factor re
159 lyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog in the Drosophi
161 Further, we show that lack of interleukin-1 (IL-1) receptor attenuates gammaherpesvirus-driven B cell
169 cessory protein (IL-1RAcP) form a functional IL-1 receptor complex that is thought to mediate most, i
170 l cells, express a functional interleukin-1 (IL-1) receptor complex and respond with NF-kappaB activa
171 a coli strains, such as CFT073, express Toll/IL-1 receptor-containing (TIR-containing) protein C (Tcp
174 h subsequent immunoglobulin E responses, and IL-1-receptor-deficient mice failed to induce iBALT form
175 (Ptpn6(DeltaPMN)) is sufficient to initiate IL-1 receptor-dependent cutaneous inflammatory disease,
177 or necrosis factor (TNF)- and interleukin-1 (IL-1) receptor-dependent activation of stellate cells an
178 ons to prevent autoimmune and interleukin-1 (IL-1) receptor-dependent, caspase-1-independent inflamma
181 esponse protein 88, and adaptor protein Toll/IL-1 receptor domain-containing adapter-inducing IFN-bet
183 hanisms dependent on and independent of Toll/IL-1 receptor domain-containing adaptor inducing IFN-bet
184 driven cytokine production we observed, Toll-IL-1 receptor domain-containing adaptor protein degradat
185 models BTK regulates the degradation of Toll-IL-1 receptor domain-containing adaptor protein, termina
186 d differentiation response gene 88, and Toll-IL-1 receptor domain-containing adaptor-inducing interfe
187 erferon-independent mechanism involving Toll-IL-1-receptor domain-containing adapter-inducing IFN-alp
188 TLR4-mediated nuclear factor-kappaB and Toll/IL-1 receptor-domain-containing adapter-inducing interfe
190 ammation after DSS colitis recovery, induced IL-1 receptor expression in subepithelial fibroblasts, a
191 toll-like receptors (TLRs) and interleukin (IL)-1 receptor family member signaling in postnatal gene
192 the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various i
193 extracellular domains of each member of the IL-1 receptor family, including the IL-36 receptor (also
198 hat MyD88, a known critical component of the IL-1 receptor I signaling pathway, plays a crucial role
200 his study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r(-/-)) or deficient in IL1-be
201 found that Trim24(-/-) T cells have reduced IL-1 receptor (IL-1R) expression, are refractory to IL-1
202 severe asthma compared with MMAs, including IL-1 receptor (IL-1R) family and nucleotide-binding olig
205 ablation or selective expression of IL-1 and IL-1 receptor (IL-1R) in either microglia or endothelia
206 targets, including cytokine signaling by the IL-1 receptor (IL-1R) pathway and inflammasome activatio
207 IL-12, and this bystander response required IL-1 receptor (IL-1R) signaling during early pulmonary i
208 e demonstrate a key role for T cell-specific IL-1 receptor (IL-1R) signals in the accumulation and su
209 Both IL-1alpha and IL-1beta ligate the same IL-1 receptor (IL-1R) that is present on nearly all cell
210 beta initiates cell signaling by binding the IL-1 receptor (IL-1R) whereas IL-1Ra acts as an antagoni
212 neas, but labeling was reduced and patchy on IL-1 receptor (IL-1R)-knockout mouse corneas (P < 0.05,
222 LSC demonstrated increased expression of the IL-1 receptors, IL-1 receptor accessory protein and IL-1
224 eceptor, SIGIRR, or TIR8) is a member of the IL-1 receptor (ILR) family with distinct structural and
225 ade of IL-1beta or genetic deficiency of the IL-1 receptor in dendritic cells (DCs) and T cells impro
227 letion in hippocampal neurons confirmed that IL-1 receptor in the hippocampus was critical for stress
231 a neutralizing antibody and macrophages from IL-1 receptor knockout mice blocked the conditioned medi
233 eta (IL-1beta), an inflammatory cytokine and IL-1 receptor ligand, has diverse activities in the brai
235 e reflected in nasal epithelium and included IL-1 receptor like 1, prostaglandin-endoperoxide synthas
236 ), which is the soluble form of interleukin (IL)-1 receptor-like 1, identifies risk in acutely decomp
239 wide association studies identified IL33 and IL-1 receptor-like 1 (IL1RL1)/IL18R1 as asthma susceptib
240 riptional analyses identified lower level of IL-1 receptor-like 1 (ST2) expression in microglia/macro
241 ) and confirmed 4 asthma risk regions: 2q12 (IL-1 receptor-like 1 [IL1RL1]), 6p21 (HLA-DQA1), 9p24 (I
242 like 3 and gasdermin B (ORMDL3-GSDMB), IL33, IL-1 receptor-like 1 and IL-18 receptor 1 (IL1RL1-IL18R1
243 of the IL-33 receptor gene Il1rl1 (encoding IL-1 receptor-like 1, also known as ST2) in ILC2p and co
245 -specific Th1/Th17 immune responses required IL-1 receptor-mediated signals independent of IL-18 and
247 at is prevented by genetic deletion of IL-1 (IL-1) receptor or apoptosis-associated speck-like protei
249 .001), toll-like receptors (TLR; p < 0.001), IL-1 receptor (p = 0.001), myeloid differentiation prima
251 r type 1 (IL-1RI) co-receptor, Toll-like and IL-1 receptor regulator (TILRR), amplifies IL-1 activati
252 including the IL-36 receptor (also known as "IL-1 receptor-related protein 2") and observed that IL-3
254 mulation of IL-1alpha or IL-1beta binding to IL-1 receptor showed distinct interaction sites that cor
255 These in vitro effects require endothelial IL-1 receptors, shown by immunofluorescence to be expres
258 sed in the Tg(CJD) hippocampus, and blocking IL-1 receptor signaling restored normal synaptic respons
259 ic inhibitor of Toll-like receptor (TLR) and IL-1 receptor signaling that prevents polarization towar
261 activation of a MyD88-dependent pathway and IL-1 receptor signaling, control of viral replication by
266 eutralizing antibody, recombinant IL-1RA, or IL-1 receptor-targeting small interfering RNA suppresses
267 which presumably distinguishes them from the IL-1 receptors that exhibit a more promiscuous ligand re
268 hermore, we show that the intracellular Toll/IL-1 receptor (TIR) domain of Nv-TLR can interact with t
269 inal death domain (DD) and a C-terminal Toll/IL-1 receptor (TIR) domain, separated by a short region.
270 r achieving LPS-inducible signaling via Toll/IL-1 receptor (TIR) domain-containing adapter-inducing i
272 ibits TLR4 signaling and interacts with Toll-IL-1 receptor (TIR) domain-containing proteins of the re
276 signaling requires interactions of the Toll/IL-1 receptor (TIR) domains of the receptor and adapter
277 elino-3 in signaling pathways emanating from IL-1 receptors, Toll-like receptors, NOD-like receptors,
278 transcriptionally upregulated by ligands of IL-1 receptor/Toll-like receptor family members via the
279 phabeta knockout (KO) mice and perioperative IL-1 receptor type 1 (IL-1R1) blockade with the drug ana
280 We report that mature IL-1 signaling at IL-1 receptor type 1 (IL-1R1) is maintained at pH 6.2, b
282 ceptors, IL-1 receptor accessory protein and IL-1 receptor type 1 (IL-1R1), and enhanced sensitivity
283 ion, pertussis toxin administration leads to IL-1 receptor type 1 (IL-1R1)-dependent IL-1beta express
284 e signaling and independent of IL-1alpha and IL-1 receptor type 1 (IL-1R1); nevertheless, IL-1alpha c
286 re mediated in part through IL-1, because an IL-1 receptor type 1 antagonist ameliorated the effects
289 lance between IL-1 and its natural inhibitor IL-1 receptor type 2 (IL1R2) in women with endometriosis
290 atherosclerotic plaques in mice lacking both IL-1 receptor type I and apolipoprotein E (Il1r1(-)/(-)A
291 n, which in turn down-regulated sequentially IL-1 receptor type I and Sema3A expression through Erk/J
294 thology was reduced in mice deficient in the IL-1 receptor Type I, but the IL-1R-/- mice were fully p
300 3s, acetate-FFAR2 augments expression of the IL-1 receptor, which boosts IL-22 secretion in response