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1 ugh expression, activation, and secretion of interleukin-18.
2 ived interferon (IFN)-a and monocyte-derived interleukin-18.
3 ity and with circulating levels of CXCL9 and interleukin-18.
4 uent release of mature interleukin-1beta and interleukin-18.
5 ponsive to stimulation by interleukin-12 and interleukin-18.
12 ingle cell RNA sequencing analysis, suggests interleukin 18 and CD95 signalling may trigger activatio
13 expression of the pro-inflammatory cytokine interleukin 18 and decreased expression of Serpin a3b, a
15 formities had significantly higher levels of interleukin 18 and IP-10 but lower levels of hepatocyte
17 ition is more strongly associated with urine interleukin 18 and kidney injury molecule 1 in children
20 ation of the cytokines interleukin-1beta and interleukin-18 and a lytic form of cell death termed pyr
21 the spleen and liver and reduced amounts of interleukin-18 and alpha/beta interferon secreted in the
24 display diminished cell death and decreased interleukin-18 and interleukin-1B production, when infec
26 inflammatory cytokines interleukin-1beta and interleukin-18 and pyroptosis, a form of phagocyte cell
27 inflammatory cytokines interleukin-1beta and interleukin-18 and pyroptotic cell death that causes the
28 the association between circulating level of interleukin-18 and systemic lupus erythematosus (SLE).
29 lation between the pro-inflammatory cytokine interleukin-18 and the anti-atherogenic adipokine adipon
30 ytes are a source of biologically functional interleukin-18 and thus are capable of playing an initia
32 nflammatory cytokines (interleukin 1beta and interleukin 18) and the antiinflammatory cytokine interl
33 peck-like protein containing a CARD), IL-18 (Interleukin-18) and IL-1beta (Interleukin- 1Beta) in obe
34 r (TNF) alpha, interleukin 1beta (IL-1beta), interleukin 18, and interleukin 6; chemokines CCL2, CCL4
36 in 6, interferon gamma-inducible protein 10, interleukin 18, and tumor necrosis factor alpha) and neg
37 MAIT cells was dependent on monocyte-derived interleukin 18, and was reduced in patients with HCV inf
38 ncluding interleukin-15, interleukin-17, and interleukin-18, and clinical trials of these agents are
39 ver-type fatty acid binding protein, urinary interleukin-18, and cystatin C) were measured in 1,635 u
41 ed lipocalin (NGAL), monomeric NGAL (mNGAL), interleukin-18, and standard biomarkers were measured at
42 had higher systemic levels of interleukin-6, interleukin-18, and tumor necrosis factor alpha than tho
44 nterleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor necrosis factor-R2 were each s
47 [CRP], Chitinase 3-like protein-1 [CHI3L1], Interleukin 18 Binding Protein [IL-18BP], soluble Tumor
48 increased C-reactive protein, ferritin, and interleukin 18 binding protein, which in turn had direct
51 s have potential implications for the use of interleukin-18 binding protein for treatment of chronic
52 by blocking its biological activity with the interleukin-18 binding protein in the murine model of se
53 rleukin-6, were randomized to receive either interleukin-18 binding protein or vehicle approximately
54 se mice with a predicted low mortality rate, interleukin-18 binding protein significantly increased m
56 IFN-gamma) receptor, IFN resistance protein, interleukin-18 binding protein, IFN-alpha/beta binding p
58 topontin (DPT), beta-crystallin B1 (CRYBB1), interleukin-18-binding protein (IL18BP) and vascular end
59 th factors, transforming growth factor beta, interleukin-18-binding protein, semaphorin, and five ser
62 kine induction (including interleukin-12 and interleukin-18), but was bereft of interferon-alpha indu
64 inflammatory cytokines interleukin-1beta and interleukin-18 by macrophages in response to alum in vit
65 of cg03636183 in F2RL3 were associated with interleukin-18 concentration (-0.11 pg/mL, 95% CI: -0.19
68 In the second stage, endogenous IL-1beta and interleukin 18 further amplify IL-36gamma synthesis.
73 5% amino acid sequence identities with human interleukin-18 (hIL-18)-binding protein (hIL-18BP), a na
74 recently shown that early administration of interleukin 18 (IL-18) after bone marrow transplantation
76 hylococcus are capable of causing release of interleukin 18 (IL-18) from keratinocytes and that S. au
78 t the deubiquitinase Cyld prevents excessive interleukin 18 (IL-18) production in the colonic mucosa
80 ly resistant A/J mice released low levels of interleukin 18 (IL-18) upon infection with Salmonella ty
81 or necrosis factor alpha (TNF-alpha) but not interleukin 18 (IL-18), convalescent myocardial inflamma
83 (6 x 10(6) CFU) resulted in the induction of interleukin 18 (IL-18), tumor necrosis factor alpha (TNF
84 alCer) and measured B cell activation during interleukin 18 (IL-18)-induced chronic inflammation.
85 me intracellular parasitic protozoa involves interleukin 18 (IL-18)-mediated interferon gamma (IFN-ga
86 ation with EPA led to a greater reduction in interleukin-18 (IL-18) (-7.0% +/- 2.8% compared with -0.
88 ls of gamma interferon and reduced levels of interleukin-18 (IL-18) and IL-10 in the serum of the Del
91 vestigated the in vitro effects of combining interleukin-18 (IL-18) and IL-2 on human lymphocytes.
92 speck-like protein containing a CARD (ASC), interleukin-18 (IL-18) and interleukin-1beta(IL-1beta) p
93 ed secretion of the proinflammatory cytokine interleukin-18 (IL-18) and multiantigen targeting could
94 y cytokines interleukin-1beta (IL-1beta) and interleukin-18 (IL-18) as well as pyroptotic cell death.
96 r viral immune-modulatory genes, encoding an interleukin-18 (IL-18) binding protein, an IL-1beta rece
102 inflammatory protein 1 beta (MIP-1beta), and interleukin-18 (IL-18) in 131 patients with chronic HCV
103 NGAL), Kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18) in cirrhotic patients with AKI.
120 munotherapy, we found that components of the interleukin-18 (IL-18) pathway are upregulated on tumour
123 stically, Tak1 activation leads to increased interleukin-18 (IL-18) production, whereas blockade of I
125 site Tbx21-CNS-3, and the expression of the interleukin-18 (IL-18) receptor; IL-18 induced T-bet exp
127 inflammasome as the major pathway leading to interleukin-18 (IL-18) release and restriction of S Typh
128 mory T cells with interleukin-12 (IL-12) and interleukin-18 (IL-18) results in tightly regulated prog
129 to limit T-cell exhaustion, and constitutive interleukin-18 (IL-18) secretion to enhance immune funct
132 proinflammatory and proatherogenic cytokine interleukin-18 (IL-18) stimulates SMC proliferation, we
135 ethyl ester (BAA473) can induce secretion of interleukin-18 (IL-18) through activation of the inflamm
137 ranscription of the proinflammatory cytokine interleukin-18 (IL-18) was significantly higher in PVAN
139 n hosts encode homologous proteins that bind interleukin-18 (IL-18) with high affinity and inhibit IL
140 tions, decreased placental bed expression of interleukin-18 (IL-18) with increased production of temp
141 th pancytopenia had sustained high levels of interleukin-18 (IL-18) with low levels of IL-18 binding
143 enolase (NSE), a marker of brain damage, and interleukin-18 (IL-18), an innate immune marker, mainly
144 ere prevalent and included gamma interferon, interleukin-18 (IL-18), and the immunosuppressive, fibro
145 e the level of Toll-like receptor 4 (TLR-4), interleukin-18 (IL-18), and uric acid as markers of the
146 ), and urinary kidney injury markers such as interleukin-18 (IL-18), connective tissue growth factor
149 phil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1)
150 RD, caspase-1, interleukin-1beta (IL-1beta), interleukin-18 (IL-18), nucleotide-binding domain, leuci
151 mphocytes activation by differentiating into interleukin-18 (IL-18)- and IL-15-producing cells in an
152 ophages activated NK cells in a contact- and interleukin-18 (IL-18)-dependent manner, whereas monocyt
153 anism in the spleen, but both pyroptosis and interleukin-18 (IL-18)-driven natural killer (NK) cell r
160 iated cytotoxicity (familial HLH) and excess interleukin-18 (IL-18; macrophage activation syndrome) p
162 CL10/interferon-inducile protein 10 [IP-10], interleukin 18 [IL-18], CCL2/monocyte chemoattractant pr
163 amma inducible protein (IFI16), and cytokine interleukin 18 (IL18) in individuals with periodontitis,
164 g inducible nitric oxide synthase (iNOS) and interleukin 18 (IL18), suggesting Hg-induced inflammator
167 enterocolitis is due to up-regulation of the interleukin-18 (IL18) signaling pathway, and pharmacolog
168 unctional polymorphisms in the gene encoding interleukin-18 (IL18), a cytokine belonging to the IL-1
170 ine levels, and messenger RNA expressions of interleukin-18 in kidney, interleukin-6, indoleamine 2,3
171 trophil gelatinase-associated lipocalin, and interleukin-18 in predicting early graft function after
172 rthermore, we demonstrated the importance of interleukin-18 in preventing alveolar macrophage endotox
175 ed with type A F. tularensis did not release interleukin-18 in vitro, a response that requires the ac
176 previously uncharacterized states such as an interleukin-18-induced polyfunctional natural killer cel
178 locyte-macrophage colony-stimulating factor, interleukin-18, interferon-gamma and possibly interleuki
179 eukin-23p40, interleukin-13, interleukin-17, interleukin-18, interferongamma, transforming growth fac
180 erging or enlarged roles for interleukin-10, interleukin-18, interleukin-9, chemokines, activation of
183 Interferon-gamma-inducing factor (IGIF, interleukin-18) is a recently described cytokine that sh
185 , ATX, and Mac2BP levels declined by week 2, interleukin 18 levels declined by the end of treatment,
187 cts suggest that cigarette smoking increases interleukin-18 levels through the decrease in DNA methyl
188 il gelatinase-associated lipocalin and serum interleukin-18 levels were not different between groups.
189 atients showed elevated NLRP3, caspase-1 and interleukin-18 messenger RNA expression and, using a mou
190 phage endotoxin tolerance through studies of interleukin-18 messenger RNA expression in il-18r-/- mic
191 r oncolytic HSV-1 vectors, expressing murine interleukin 18 (mIL-18), soluble murine B7-1 [B7-1-immun
192 oluble CD163 (sCD163), interleukin 6 (IL-6), interleukin 18, monocyte chemoattractant protein (MCP-1)
193 nterleukin-6, interleukin-8, interleukin-10, interleukin-18, monocyte chemotactic protein-1, high-mob
195 selected non-bone marrow derived skin cells, interleukin-18 mRNA is constitutively expressed by human
197 in use, and additional agents that modulate interleukin-18, myeloid-related proteins 8 and 14, natur
198 ostoperative (0-6 hours after surgery) urine interleukin 18, neutrophil gelatinase-associated lipocal
199 stically, Notch4 suppressed the induction by interleukin-18 of amphiregulin, a cytokine necessary for
200 and the decreases in both CRP (P = .01) and interleukin 18 (P = .02) levels were smaller in underwei
201 The roles of the interleukin 1 (IL-1) and interleukin 18 pathways in host defense are well establi
202 and activation of the ATM/YAP1/precursor of interleukin 18 (pro-IL-18) pathway in the intestinal epi
206 y NK cells in response to interleukin-12 and interleukin-18, providing a mechanistic link between CD3
210 ludes the type I interleukin-1 receptor, the interleukin-18 receptor, and a growing family of Toll-li
211 eins, including Nt-proBNP, thrombospondin-2, interleukin-18 receptor, gelsolin, and activated C5.
212 ooth muscle cells (VSMCs) express functional interleukin-18 receptors (IL-18Rs), composed of alpha an
213 (>0.3 x 10(9) /L) at screening and low serum interleukin-18 relative change at pre-treatment baseline
214 nts with high blood eosinophils or low serum interleukin-18 response are potential subgroups for furt
215 nts with high blood eosinophils or low serum interleukin-18 response are potential subgroups for furt
216 e knockout of a single Toll-like receptor or interleukin 18 resulted only in minor impairment of bact
217 -) mice were given injections of recombinant interleukin 18 (rIL18) or saline (control) during DSS ad
220 on of vascular endothelial growth factor and interleukin-18 signaling in dermatomyositis keratinocyte
223 s of proinflammatory cytokines TNF-alpha and interleukin 18 than the HEV-infected pigs without detect
224 min-D-dependent pyroptosis and processing of interleukin-18, thereby destroying the replicative niche
225 d exposure to inflammatory mediators such as interleukin-18, these cells rapidly release type 2 cytok
226 by inflammatory markers ranged from 1.5% for interleukin 18 to 14.2% for C-reactive protein, and 16.1
228 nes, including the key Th1-inducing cytokine interleukin-18, upon Salmonella challenge than those fro
229 ain replicating HCV and respond by producing interleukin-18 via the inflammasome and by activating NK
232 ome in monocytes, or after neutralization of interleukin-18, which is regulated by the inflammasome.