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1 a and IL-1beta, both of which signal through IL-1 receptor.
2 mphocytes) but not in mice deficient for the IL-1 receptor.
3 onal priming effect that was mediated by the IL-1 receptor.
4 tivated TNF receptors but not with activated IL-1 receptors.
5 pendent on activation of beta-adrenergic and IL-1 receptors.
6 diates signaling downstream of the IL-18 and IL-1 receptors.
7 onal toll-like receptor 4 and interleukin-1 (IL-1) receptors.
8 stinal lamina propria lymphocytes expressing IL-1 receptor 1 (IL-1R1) is the lymphoid tissue inducer
9              Increased lethality depended on IL-1 receptor 1 (IL-1R1) signaling but not adaptive immu
10        Mice lacking IL-6 receptor (IL-6R) or IL-1 receptor 1 (IL-1R1) specifically on B cells have a
11 ion and controlled cytokine production in an IL-1 receptor 1 (IL-1R1)-independent way.
12  gene expression patterns, we identified the IL-1 receptor 1 (IL1R1) as a direct target of miR-BHRF1-
13                        Although knockdown of IL-1 receptor 1 did not attenuate lymphocytic infiltrati
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
16 r necrosis, which increased its affinity for IL-1 receptor 1.
17 ptor-1 knockout (TNFRKO), and interleukin-1 (IL-1) receptor-1 knockout (IL1RKO) mice as a means of fu
18 st cell types examined expressed a cytosolic IL-1 receptor 2 (IL-1R2) whose binding to pro-IL-1alpha
19        In a joint analysis of all 4 cohorts, IL-1 receptor 2 (IL1R2) and Toll-like receptor 1 (TLR1)
20 ng requires the type 1 IL-1 receptor and the IL-1 receptor accessory protein (IL-1RAcP) as a receptor
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
27 tor (IL-36R) and a shared subunit, IL-1RAcP (IL-1 receptor accessory protein).
28 plexed with the newly discovered alternative IL-1 receptor accessory protein, IL-1RAcPb.
29 on of several markers such as interleukin-1 (IL-1) receptor accessory protein (IL1RAP), CD99, T-cell
30 more severe renal epithelial cell damage via IL-1 receptor activation in coculture compared with WT m
31                        Mice deficient in the IL-1 receptor also had reduced levels of circulating P-s
32 A fibrotic infrapatellar fat pad express the IL-1 receptor and on exposure to IL-1alpha polarize to a
33 H2/TH17 cells expressed higher levels of the IL-1 receptor and phospho-p38 mitogen-activated protein
34                                Variations in IL-1 receptor and receptor antagonist expression, Ikappa
35     Carotid body glomus cells also expressed IL-1 receptor and responded to application of IL-1beta w
36           IL-1 signaling requires the type 1 IL-1 receptor and the IL-1 receptor accessory protein (I
37 l for NF-kappaB activation via TNF receptor, IL-1 receptor and toll-like receptor 4.
38 tokine receptors, but rather, indirectly via IL-1 receptors and TNF receptors being expressed on glia
39             The effect of daily interleukin (IL)-1 receptor antagonist before stress on anhedonia was
40  IL-1beta following the severe stressor with IL-1 receptor antagonist (10 mug, intracerebroventricula
41                  Mice given injections of an IL-1 receptor antagonist (anakinra) or antibodies to dep
42  IL-22 and IL-17 was not that of the classic IL-1 receptor antagonist (anakinra), because low concent
43  achieved a complete response to recombinant IL-1 receptor antagonist (anakinra).
44 y brain-specific overexpression of the human IL-1 receptor antagonist (hIL1ra(Ast)(+/+) mice) leads t
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
47 r LPS stimulated anti-inflammatory IL-10 and IL-1 receptor antagonist (IL-1Ra) expression in mouse li
48               Systemic blockade of IL-1 with IL-1 receptor antagonist (IL-1Ra) fully reversed infecti
49 AT1 downregulation, whereas incubation of an IL-1 receptor antagonist (IL-1ra) in EAE slices reduced
50                   Treatment with recombinant IL-1 receptor antagonist (IL-1RA) inhibited IL-1 signali
51               Supplementing cultures with an IL-1 receptor antagonist (IL-1Ra) modulated the DRlyp/ly
52 y of the administration of recombinant human IL-1 receptor antagonist (IL-1ra) on biomarkers of infla
53 nction, whereas higher circulating levels of IL-1 receptor antagonist (IL-1RA), an endogenous inhibit
54 pha, of interleukin-1beta (IL-1beta), and of IL-1 receptor antagonist (IL-1ra), and correlated cytoki
55                  IL-1alpha, IL-1beta, IL-18, IL-1 receptor antagonist (IL-1RA), and IL-8 levels were
56 knockout (IL-1R1 KO) mice, in mice receiving IL-1 receptor antagonist (IL-1RA), and in mice given the
57 2) fragments of anti-CD3 mAb with or without IL-1 receptor antagonist (IL-1RA), or anti-IL-1beta mAb.
58 has co-evolved with a competitive inhibitor, IL-1 receptor antagonist (IL-1Ra).
59  of antiinflammatory molecules, specifically IL-1 receptor antagonist (IL-1Ra).
60  impairs production of the anti-inflammatory IL-1 receptor antagonist (IL-1Ra).
61  induction of the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1Ra, 16 +/- 1.7 ng/mL, mean
62            Mice were treated acutely with an IL-1 receptor antagonist (IL-1Ra; 100 mg/kg, s.c.) or ve
63 pression, which, in turn, down-regulated the IL-1 receptor antagonist (IL1Ra) expression.
64 evoked inflammatory stress to measure plasma IL-1 receptor antagonist (IL1RA) following low-dose Food
65          rs315952 in the IL1RN gene encoding IL-1 receptor antagonist (IL1RA) replicated its associat
66        We compared sequences of IL-1beta and IL-1 receptor antagonist (IL1RN), which is an IL-1beta h
67  (P = 0.001), TNF receptor-2 (P < 0.01), and IL-1 receptor antagonist (P = 0.02) concentrations were
68 luble TNF receptor-1 (sTNFR1; p < .001), and IL-1 receptor antagonist (p value in mania < .001 and eu
69 ased plasma interleukin (IL)-6, IL-1beta and IL-1 receptor antagonist (R=-0.33 to -0.36, P<0.05).
70                           Conversely, higher IL-1 receptor antagonist (ra) levels were found in healt
71 mation index ratio of interleukin (IL)-1beta/IL-1 receptor antagonist (ra) using enzyme-linked immuno
72 tin, and IL-1beta and its antagonist soluble IL-1 receptor antagonist (sIL-1Ra); depletion of corneal
73 terleukin [IL]-1 beta [IL-1beta], rs1143623; IL-1 receptor antagonist [IL-1ra], rs4251961; IL-10, rs1
74                 Blockade of IL-1beta with an IL-1 receptor antagonist abolished obesity-induced AHR a
75  breast cancer, we demonstrate here that the IL-1 receptor antagonist anakinra abrogates IL-22 produc
76  neutralization of IL-1 and IL-18, using the IL-1 receptor antagonist anakinra and anti-IL-18 antibod
77 ons in acute-phase hsCRP production with the IL-1 receptor antagonist anakinra and the IL-6 receptor
78 e activation to (1) assess the safety of the IL-1 receptor antagonist anakinra in conjunction with in
79 open-label, single-arm clinical trial of the IL-1 receptor antagonist anakinra in corticosteroid-resi
80 hibitory effect on IL-1beta secretion by the IL-1 receptor antagonist anakinra in phagocytes of patie
81                                    Last, the IL-1 receptor antagonist anakinra protected animals agai
82 Similarly, intrathecal administration of the IL-1 receptor antagonist anakinra restored locomotor fun
83                      Increased expression of IL-1 receptor antagonist and Glut4 in skeletal muscles a
84            Conversely, the anti-inflammatory IL-1 receptor antagonist and IL-4 were decreased in RA c
85 nd augmented production of anti-inflammatory IL-1 receptor antagonist and vascular endothelial growth
86 nary arteritis and evaluated the efficacy of IL-1 receptor antagonist as a potential treatment.
87     Antagonism of endogenous IL-1alpha using IL-1 receptor antagonist blocked gel contraction by SSc
88 ockade of endothelial IL-1beta receptor with IL-1 receptor antagonist completely suppressed endotheli
89 otoxin concentrations correlated with sputum IL-1 receptor antagonist concentrations (r = 0.510, P <
90 RNA against NLRP3, recombinant IL-1beta, and IL-1 receptor antagonist confirmed the role of NLRP3 inf
91 ized that a synonymous coding variant in the IL-1 receptor antagonist gene (IL1RN), rs315952, previou
92            Indeed, neutralization of IL-1 by IL-1 receptor antagonist has recently been shown to pote
93                           The effects of the IL-1 receptor antagonist IL-1ra against the aggressive/i
94 ivated NLRC4 for sustained production of the IL-1 receptor antagonist IL-1Ra, which restrained NLRP3
95 sRNA-dependent production of IL-1, TSLP, and IL-1 receptor antagonist in NHBE cells was regulated by
96 -1alpha (but not IL-1beta) or application of IL-1 receptor antagonist inhibited platelet-induced endo
97 t of disease mimic organotypic cultures with IL-1 receptor antagonist led to a dose-dependent decreas
98                       Neonatal therapy using IL-1 receptor antagonist preserves choroid and prevents
99         Furthermore, daily injections of the IL-1 receptor antagonist prevented LCWE-mediated coronar
100                                 Anakinra, an IL-1 receptor antagonist protein, inhibited BAL TH2/TH17
101                               Treatment with IL-1 receptor antagonist reduced hypoxia and slightly, b
102 binant human IL-1beta monoclonal antibody or IL-1 receptor antagonist resulted in a dose- and time-de
103 n IL-1beta neutralizing antibody or specific IL-1 receptor antagonist revealed the primary involvemen
104 ss, and intracerebroventricular injection of IL-1 receptor antagonist reverted both effects.
105 ine induced by interferon-gamma (CXCL9), and IL-1 receptor antagonist to an extent in proportion to t
106 the human recombinant form of the endogenous IL-1 receptor antagonist used to treat rheumatoid arthri
107 ermis may have a role in dermal fibrosis, an IL-1 receptor antagonist was administered locally to hea
108 otactic protein 1, interleukin-6 (IL-6), and IL-1 receptor antagonist were moderately elevated.
109 s etanercept (TNFalpha inhibitor), anakinra (IL-1 receptor antagonist), prednisone (NFkappaB transloc
110 se of anti-inflammatory mediators (IL-10 and IL-1 receptor antagonist).
111  periodic syndromes) and DIRA (deficiency of IL-1 receptor antagonist).
112  inhibitor, or blocking of IL-1 signaling by IL-1 receptor antagonist, abrogated the Th17-promoting e
113                    With the exception of the IL-1 receptor antagonist, all IL-1 family cytokines lack
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  with the IL-1 blocker anakinra (recombinant IL-1 receptor antagonist, Kineret(R), Swedish Orphan Bio
117 ved apocynin to inhibit NADPH oxidase (NOX), IL-1 receptor antagonist, or IL-18 binding protein to pr
118 nged with PMN-SA produced more IL-8 and less IL-1 receptor antagonist, TNF-alpha, activated caspase-1
119  expression of IL-1R-associated kinase M and IL-1 receptor antagonist, which are negative regulators
120 ing in life-long improved visual function in IL-1 receptor antagonist-treated OIR animals.
121 nd the anti-inflammatory cytokines IL-10 and IL-1 receptor antagonist.
122 he latter was abolished after treatment with IL-1 receptor antagonist.
123 al resolution was achieved with anakinra, an IL-1 receptor antagonist.
124 y lesions in this KD mouse model, blocked by IL-1 receptor antagonist.
125 ymphopoietin (TSLP) and was enhanced by anti-IL-1 receptor antagonist.
126 erum concentrations of the counterregulatory IL-1 receptor antagonist.
127 tokines, such as interleukin (IL)-10 and the IL-1 receptor antagonist.
128 eated five PFAPA patients with a recombinant IL-1 receptor antagonist.
129 poE(-/-) and ApoE(-/-)/IL-1R1(-/-) mice with IL-1-receptor antagonist prevented progression of the PA
130 ocal treatment with anti-TNF-alpha antibody, IL-1-receptor antagonist, or indomethacin.
131 n postnatal development and investigated two IL-1 receptor antagonists, the competitive inhibitor ana
132  and can be suppressed by injections of anti-IL-1 receptor antibody.
133                                              IL-1 receptor appears to be a marker of neutrophilic inf
134 ifferentiation primary response gene 88) and IL-1 receptor-associated kinase (IRAK) 1/4 inhibitors, o
135 strated deficient TLR4-induced activation of IL-1 receptor-associated kinase (IRAK) 4, IRAK1, and TAN
136 al modifications and signalosome assembly of IL-1 receptor-associated kinase (IRAK) 4, IRAK1, TNF rec
137 f various innate immune receptors results in IL-1 receptor-associated kinase (IRAK)-1/IRAK-4-mediated
138 is and depends on the TLR-signaling molecule IL-1 receptor-associated kinase (IRAK-1) and its kinase
139 a greatly up-regulated the protein levels of IL-1 receptor-associated kinase (IRAK-1) and tumor-necro
140 itro, reducing levels of the adaptor kinases IL-1 receptor-associated kinase 1 (IRAK-1) and TNF recep
141 guanine nucleotide exchange factor VAV-1 and IL-1 receptor-associated kinase 1 (IRAK-1), respectively
142 at Tbeta4 treatment suppressed expression of IL-1 receptor-associated kinase 1 (IRAK1) and tumor necr
143 S100A7, S100A8, and S100A9 (S100A7/8/9), and IL-1 receptor-associated kinase 1 (IRAK1) establish a re
144 ike receptor (TLR4) signaling first mediates IL-1 receptor-associated kinase 1 (IRAK1) nuclear transl
145 roduction via binding to and phosphorylating IL-1 receptor-associated kinase 1 (IRAK1), leading to IR
146 R-146a diminished or enhanced, respectively, IL-1 receptor-associated kinase 1 expression and induced
147 actor 7 gene expression and rapidly degraded IL-1 receptor-associated kinase 1 expression in plasmacy
148  adaptor protein (TIRAP), and the downstream IL-1 receptor-associated kinase 1, IL-1 receptor-associa
149 ession of IL-25 and IL-33 by upregulation of IL-1 receptor-associated kinase 1, transforming growth f
150 recruitment domain-containing protein 10 and IL-1 receptor-associated kinase 1.
151 t domain adaptor inducing IFN-beta (CARDIF), IL-1 receptor-associated kinase 4 (IRAK4), IkappaB kinas
152 he TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor-associated kinase 4 [IRAK-4], TLR3, UNC-93
153 ownstream IL-1 receptor-associated kinase 1, IL-1 receptor-associated kinase 4, and TNF receptor-asso
154                                              IL-1 receptor-associated kinase M (IRAK-M) negatively re
155 nhibitor of NF-kappaB activation 3 (ABIN-3), IL-1 receptor-associated kinase M (IRAK-M), suppressor o
156  characterize an X chromosome-linked IRAK-1 (IL-1 receptor-associated kinase) polymorphism as an alte
157                                              IL-1 receptor-associated kinase-M (IRAK-M) is a macropha
158 s potentiation is mediated by a reduction in IL-1 receptor-associated kinase-M, a negative regulator
159 mune components such as Toll-like receptors, IL-1 receptor-associated kinase/tumor necrosis factor re
160                                          The IL-1 receptor-associated kinases (IRAKs) are key regulat
161 effects of stimulating or inhibiting the TLR/IL-1 receptor-associated kinases IRAK-1 and IRAK-4 in me
162              Expression and/or activation of IL-1 receptor-associated protein kinase (IRAK), TNF rece
163                               Interleukin 1 (IL-1) receptor-associated kinase (IRAK)-M is a proximal
164 lyubiquitination of Pelle, an interleukin-1 (IL-1) receptor-associated kinase homolog in the Drosophi
165                               Interleukin 1 (IL-1) receptor-associated kinases (IRAKs) are serine/thr
166                                              IL-1 receptor blockade may provide a promising strategy
167                  This unique approach limits IL-1 receptor blockade to sites of inflammation, while s
168 ing CGD patients who had severe colitis with IL-1 receptor blockade using anakinra.
169 al conditions in CGD that can be restored by IL-1 receptor blockade.
170 , comparable in extent to that obtained upon IL-1 receptor blockade.
171   Neutralization of IL-23 or blockade of the IL-1 receptor, but not IL-6 neutralization, abrogated eg
172 cessory protein (IL-1RAcP) form a functional IL-1 receptor complex that is thought to mediate most, i
173 l cells, express a functional interleukin-1 (IL-1) receptor complex and respond with NF-kappaB activa
174 a coli strains, such as CFT073, express Toll/IL-1 receptor-containing (TIR-containing) protein C (Tcp
175                                Additionally, IL-1 receptor-deficient mice show an increase in RABV pa
176                 Both caspase-1-deficient and IL-1 receptor-deficient mice were protected from LCWE-in
177 mice was completely ablated by crossing with IL-1 receptor-deficient or adaptor molecule ASC-deficien
178 h subsequent immunoglobulin E responses, and IL-1-receptor-deficient mice failed to induce iBALT form
179 and the adapter proteins each contain a Toll/Il-1 receptor domain (TIR domain).
180           The R753Q polymorphism in the Toll-IL-1 receptor domain of Toll-like receptor 2 (TLR2) has
181 esponse protein 88, and adaptor protein Toll/IL-1 receptor domain-containing adapter-inducing IFN-bet
182 hanisms dependent on and independent of Toll/IL-1 receptor domain-containing adaptor inducing IFN-bet
183          TLR4 and TLR3 can both use the 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 L-1 receptor family member contains the Toll-IL-1-receptor domain.
189 TLR4-mediated nuclear factor-kappaB and Toll/IL-1 receptor-domain-containing adapter-inducing interfe
190                                   Since Toll-IL-1-receptor domains are functional for both receptor f
191                                    TIR (Toll/IL-1 receptor) domains mediate interactions between TLR
192 ammation after DSS colitis recovery, induced IL-1 receptor expression in subepithelial fibroblasts, a
193  toll-like receptors (TLRs) and interleukin (IL)-1 receptor family member signaling in postnatal gene
194                The cytosolic segment of each IL-1 receptor family member contains the Toll-IL-1-recep
195  IL-1 family members that signal through the IL-1 receptor family members IL-1Rrp2 (IL-1RL2) and IL-1
196 the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various i
197  extracellular domains of each member of the IL-1 receptor family, including the IL-36 receptor (also
198 orphan members of the IL-1 ligand family and IL-1 receptor family, respectively.
199 oll-like receptors (TLRs) and interleukin-1 (IL-1) receptor family members.
200                             Mice with global IL-1 receptor gene knockout or central IL-6 receptor kno
201        Expression of interleukin 23 (IL-23), IL-1 receptor I (IL-1RI), IL-17R, tissue inhibitors of m
202 hat MyD88, a known critical component of the IL-1 receptor I signaling pathway, plays a crucial role
203                 Here we demonstrate that the IL-1 receptor IL-1R1 was selectively expressed by a subp
204 deficient of IL-1beta (IL-1beta knockout) or IL-1 receptor (IL-1R knockout; n=10 each).
205 his study, we observed that mice lacking the IL-1 receptor (IL-1R) (IL1r(-/-)) or deficient in IL1-be
206  found that Trim24(-/-) T cells have reduced IL-1 receptor (IL-1R) expression, are refractory to IL-1
207  severe asthma compared with MMAs, including IL-1 receptor (IL-1R) family and nucleotide-binding olig
208                               Members of the IL-1 Receptor (IL-1R) family include six receptor chains
209                 Interleukin-1 (IL-1) and the IL-1 receptor (IL-1R) family play an important role in t
210  IL-12, and this bystander response required IL-1 receptor (IL-1R) signaling during early pulmonary i
211 e demonstrate a key role for T cell-specific IL-1 receptor (IL-1R) signals in the accumulation and su
212  Both IL-1alpha and IL-1beta ligate the same IL-1 receptor (IL-1R) that is present on nearly all cell
213 beta initiates cell signaling by binding the IL-1 receptor (IL-1R) whereas IL-1Ra acts as an antagoni
214                   Wild-type (WT), TLR9(-/-), IL-1 receptor (IL-1R)(-/-), and MyD88(-/-) mice were fed
215 neas, but labeling was reduced and patchy on IL-1 receptor (IL-1R)-knockout mouse corneas (P < 0.05,
216                   Thus, our observation that IL-1 receptor (IL-1R)-mediated signals were still requir
217 involving the Toll-like receptors (TLRs) and IL-1 receptor (IL-1R).
218 cal effects of IL-1beta are mediated through IL-1 receptor (IL-1R).
219                                   The type 1 IL-1 receptor (IL-1R1) and the IL-1 receptor accessory p
220                             IL-1beta, type I IL-1 receptor (IL-1R1), and IL-1 receptor antagonist (IL
221 thological effects in the CNS through type I IL-1 receptor (IL-1R1).
222  specifically binds to TNF and to the type I IL-1 receptor (IL-1RI).
223 LSC demonstrated increased expression of the IL-1 receptors, IL-1 receptor accessory protein and IL-1
224  1 (MAV-1) infection, using mice lacking the IL-1 receptor (Il1r1(-/-) mice).
225 eceptor, SIGIRR, or TIR8) is a member of the IL-1 receptor (ILR) family with distinct structural and
226 ade of IL-1beta or genetic deficiency of the IL-1 receptor in dendritic cells (DCs) and T cells impro
227 he development of POI required activation of IL-1 receptor in nonhematopoietic cells.
228 dney from fibrosis by limiting activation of IL-1 receptors in the kidney.
229  Our data suggest that signaling through the IL-1 receptor is protective, whereas signaling through t
230 a neutralizing antibody and macrophages from IL-1 receptor knockout mice blocked the conditioned medi
231  clearance, deficiency in the interleukin 1 (IL-1) receptor led to a significant impairment.
232 eta (IL-1beta), an inflammatory cytokine and IL-1 receptor ligand, has diverse activities in the brai
233                       Here we chimerized two IL-1 receptor ligands, IL-1beta and IL-1Ra, to create an
234 ated with an IL-13-induced TH2 signature and IL-1 receptor-like 1 (IL1RL1) mRNA expression.
235                 Two of these genes, IL33 and IL-1 receptor-like 1 (IL1RL1), act in one signal transdu
236 wide association studies identified IL33 and IL-1 receptor-like 1 (IL1RL1)/IL18R1 as asthma susceptib
237 ) and confirmed 4 asthma risk regions: 2q12 (IL-1 receptor-like 1 [IL1RL1]), 6p21 (HLA-DQA1), 9p24 (I
238 like 3 and gasdermin B (ORMDL3-GSDMB), IL33, IL-1 receptor-like 1 and IL-18 receptor 1 (IL1RL1-IL18R1
239 exhibited increased release of IL-1alpha and IL-1 receptor -mediated G-CSF production.
240 iciency of Psgl-1 is associated with reduced IL-1 receptor-mediated adhesive properties of the endoth
241 -specific Th1/Th17 immune responses required IL-1 receptor-mediated signals independent of IL-18 and
242  the activity of the MPs and blockade of the IL-1 receptor on endothelial cells decreased MP-dependen
243 R4 expression by hematopoietic cells and the IL-1 receptor on radioresistant cells.
244              Pharmacologic disruption of CNS IL-1 receptor or IL-6 biological activity attenuated ano
245 at is prevented by genetic deletion of IL-1 (IL-1) receptor or apoptosis-associated speck-like protei
246        In inflammation-induced skin cancers, IL-1 receptor- or caspase-1-deficient mice, or mice spec
247 .001), toll-like receptors (TLR; p < 0.001), IL-1 receptor (p = 0.001), myeloid differentiation prima
248       The combined signaling from the TNF or IL-1 receptors promotes maximal lung inflammation that m
249                Further studies revealed that IL-1 receptor (R)1 signaling was required for IL-17A-dep
250 r type 1 (IL-1RI) co-receptor, Toll-like and IL-1 receptor regulator (TILRR), amplifies IL-1 activati
251 including the IL-36 receptor (also known as "IL-1 receptor-related protein 2") and observed that IL-3
252 tiated by dimerization of intracellular Toll/IL-1 receptor resistance (TIR) domains.
253   These in vitro effects require endothelial IL-1 receptors, shown by immunofluorescence to be expres
254                             Silencing of the IL-1 receptor signaling in the central nervous system by
255 ction of hemolysin, which required NLRP3 and IL-1 receptor signaling in vivo.
256 sed in the Tg(CJD) hippocampus, and blocking IL-1 receptor signaling restored normal synaptic respons
257 ic inhibitor of Toll-like receptor (TLR) and IL-1 receptor signaling that prevents polarization towar
258                                              IL-1 receptor signaling via the transcription factors Ah
259 IRAK-1), an essential component of Toll-like/IL-1 receptor signaling.
260                               Interleukin-1 (IL-1) receptor signaling is necessary for control of Myc
261 ial effects in treating PAH, and alternative IL-1-receptor signaling in the lung may be important in
262  protein that mediates toll and interleukin (IL)-1 receptor signalling, and the discovery of highly r
263 eceptor-deficient macrophages is mediated by IL-1 receptor stimulation in the kidney.
264 rk1/2 following stimulation of the Toll-like/IL-1 receptor superfamily.
265 which presumably distinguishes them from the IL-1 receptors that exhibit a more promiscuous ligand re
266  acid substitution, L265P, in the MYD88 Toll/IL-1 receptor (TIR) domain at an evolutionarily invarian
267 that mimic the conserved BB-loop in the Toll/IL-1 receptor (TIR) domain of MyD88.
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
271          Toll like receptors (TLRs) use Toll-IL-1 receptor (TIR) domain-containing adapters, such as
272 ibits TLR4 signaling and interacts with Toll-IL-1 receptor (TIR) domain-containing proteins of the re
273 distinct parts of the IL-1RI regulatory Toll IL-1 receptor (TIR) domain.
274                                     The Toll/IL-1 receptor (TIR) domains are crucial innate immune si
275                                     The Toll/IL-1 receptor (TIR) domains are crucial signaling module
276  signaling requires interactions of the Toll/IL-1 receptor (TIR) domains of the receptor and adapter
277 signaling pathways via a Toll-interleukin 1 (IL-1) receptor (TIR) domain.
278 elino-3 in signaling pathways emanating from IL-1 receptors, Toll-like receptors, NOD-like receptors,
279  transcriptionally upregulated by ligands of IL-1 receptor/Toll-like receptor family members via the
280      We report that mature IL-1 signaling at IL-1 receptor type 1 (IL-1R1) is maintained at pH 6.2, b
281         Both Toll-like receptor 2 (TLR2) and IL-1 receptor type 1 (IL-1r1) upstream of MyD88 have bee
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
285       Our earlier work demonstrates that the IL-1 receptor type 1 (IL-1RI) co-receptor, Toll-like and
286                                   Studies in IL-1 receptor type 1 knockout mice indicated that the in
287 r antagonist (IL-1Ra) and the decoy receptor IL-1 receptor type 2 (IL-1R2).
288 lance between IL-1 and its natural inhibitor IL-1 receptor type 2 (IL1R2) in women with endometriosis
289 atherosclerotic plaques in mice lacking both IL-1 receptor type I and apolipoprotein E (Il1r1(-)/(-)A
290 n, which in turn down-regulated sequentially IL-1 receptor type I and Sema3A expression through Erk/J
291 onal Par2 expression to repress sequentially IL-1 receptor type I and Sema3A expression.
292 kine signaling, including the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor type II.
293 thology was reduced in mice deficient in the IL-1 receptor Type I, but the IL-1R-/- mice were fully p
294 the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor type II.
295 ehavior associated with RSD did not occur in IL-1 receptor type-1 knock-out (IL-1R1(KO)) mice.
296  social defeat increased c-Fos activation in IL-1 receptor type-1-deficient mice, but did not promote
297 glia activation in the absence of functional IL-1 receptor type-1.
298                  An absence of IL-17A or the IL-1 receptor was associated with reduced neutrophil rec
299            A robust increase in IL-1beta and IL-1 receptor were detected after TBI.
300        BALB/c mice deficient in NLRC4 or the IL-1 receptor were highly susceptible to orogastric but

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