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1 nterleukin 4, interleukin 5, interleukin 10, interleukin 13).
2 acrophages, polarized with interleukin-4 and interleukin-13.
3 beta1, connective tissue growth factor, and interleukin-13.
4 of CD4+ T cells producing interleukin-4 and interleukin-13.
5 canonical T(H)2 cytokines interleukin-4 and interleukin-13.
6 lic esophagitis, including interleukin-5 and interleukin-13.
7 tly reduced Th2 cytokines, interleukin-4 and interleukin-13.
8 h-2-type cytokines such as interleukin-4 and interleukin-13.
9 nes, in the first instance interleukin-4 and interleukin-13.
10 0, 95% CI 0.30-0.81, interaction p=0.02) and interleukin-13 (0.52, 0.34-0.82, 0.0005) response to tet
12 ansforming growth factor beta1 (TGFbeta1) or interleukin-13, although active TGFbeta1 was present loc
13 ome 11, in a region containing the genes for interleukin 13 and granulocyte/macrophage-colony-stimula
15 d the levels of predicted targets, including interleukin-13 and 3 tumor necrosis factor receptors (TN
16 f a recombinant chimeric protein composed of interleukin-13 and a mutated form of Pseudomonas exotoxi
17 id cells (ILCs), resulting in suppression of interleukin-13 and hallmark features of the allergic res
18 egulator analysis, we observed inhibition of interleukin-13 and IFN-gamma and dysregulation of biolog
19 ined elevated levels of interferon-gamma and interleukin-13 and increased levels of CCR1 ligands CCL3
22 onchoalveolar lavage eosinophil counts, lung interleukin-13 and interleukin-5 levels, and airway hype
25 ids in HMC-1 cells resulted in activation of interleukin-13 and tumor necrosis factor-alpha promoters
26 of two Th-2 cytokines (i.e., interleukin-5, interleukin-13) and one Th-1 cytokine (i.e., interferon-
27 in the concentration of interferon gamma and interleukin 13, and in the amount of proliferation betwe
29 ate regulator of three genes, interleukin-4, interleukin-13, and interleukin-5, spread over 120 kilob
30 yte-macrophage colony-stimulating factor and interleukin-13, and natural killer cell enhancing factor
31 phageal eosinophilia and that interleukin-4, interleukin-13, and STAT6 contributed to a lesser extent
32 pe 2 (T2) inflammation through the action of interleukin-13, and that the interferon response to resp
33 tionally distinct sensory neurons, including interleukin-13- and leukotriene-responsive Nmu-hi cells
39 ssion, and the addition of interleukin-4 and interleukin-13 blockade with dupilumab resulted in rapid
40 tured mast cells secreted greater amounts of interleukin-13 but much less MIP-1beta and interleukin-6
41 tumorigenicity (ST2)-dependent production of interleukin-13 by eosinophils in the hepatoprotection ag
42 cently, we have shown that interleukin-4 and interleukin-13 can independently induce human macrophage
43 cells and that these cytokines, particularly interleukin-13, can act directly on airway smooth muscle
44 also led to a decrease in interleukin-4 and interleukin-13 concentrations, which drive the Th2 respo
45 childhood TBM based on CSF concentrations of interleukin 13 (cutoff value, 37.26 pg/mL), vascular end
46 LPS exposure, and increasing PI3K activity (interleukin-13) decreased release of prostaglandin E2 af
51 ytes and mediators, including interleukin-5, interleukin-13, eotaxin, prostanoids and cysteinyl leuko
52 to treatment is heterogeneity in the role of interleukin-13 expression in the clinical asthma phenoty
53 ntly been reported for the interleukin-4 and interleukin-13 genes (IL4 and IL13) with the interleukin
55 lonal antibody that blocks interleukin-4 and interleukin-13, has shown efficacy in patients with asth
56 or 24 of 27 analytes, with interleukin-8 and interleukin-13 higher in AML and vascular endothelial gr
57 uman natural killer (NK) cells revealed that interleukin 13 (IL-13) and interferon gamma (IFN-gamma)
63 to the lung, bred these mice with CC10-rtTA-interleukin 13 (IL-13) mice in which IL-13 was overexpre
65 ad elevated serum levels of the Th2 cytokine interleukin 13 (IL-13) on day 6 after T-cell transfer co
66 tain their function and selectively maintain interleukin 13 (IL-13) production via increased acquisit
67 cells in situ exhibit on their surfaces the interleukin 13 (IL-13) receptor designated IL13Ralpha2.
68 The level of the anti-inflammatory cytokine interleukin 13 (IL-13) was lower in the serum and lungs
69 Type 2 helper T cells (TH2 cells) produce interleukin 13 (IL-13) when stimulated by papain or hous
70 human airway epithelia with the Th2 cytokine interleukin 13 (IL-13), examining how this affected DPP4
71 fact, liver fibrosis, which is dependent on interleukin 13 (IL-13), increased by a factor of more th
73 (IL-4)(-/-) BALB/c mice have indicated that interleukin 13 (IL-13), whose receptor shares the IL-4Ra
74 ting an activated phenotype and induction of interleukin 13 (IL-13)- and GATA3-expressing Th2-type CD
75 ix metalloproteinase 2 (MMP2), as part of an interleukin 13 (IL-13)-dependent regulatory loop, dampen
76 previously unknown pathway that required the interleukin 13 (IL-13)-IL-33 axis and cells of the non-T
77 -2 (Th2) [increased interleukin 5 (IL-5) and interleukin 13 (IL-13)] and T regulatory type-1 (Tr1) (I
78 In addition, this allergic response required interleukin-13 (IL-13) (the response was absent in IL-13
79 chanism dependent on interleukin-4 (IL-4) or interleukin-13 (IL-13) activation of signal transducer a
81 (CB) is a recombinant protein consisting of interleukin-13 (IL-13) and a truncated form of Pseudomon
82 reater airway necrosis, and higher levels of interleukin-13 (IL-13) and airway mucin expression than
85 (STAT6) is a critical up-stream mediator of interleukin-13 (IL-13) and IL-4 signaling and is constit
87 re of allergic lung disease, is regulated by interleukin-13 (IL-13) as well as the eotaxin chemokines
89 te, suppression depended on the secretion of interleukin-13 (IL-13) by iNKT cells because an antibody
90 roup 2 innate lymphoid cells (ILC2s) release interleukin-13 (IL-13) during protective immunity to hel
91 have clearly demonstrated that the cytokine interleukin-13 (IL-13) effectively targets glioblastoma
95 t ITLN1 gene expression is highly induced by interleukin-13 (IL-13) in a subset of metaplastic MUC5AC
97 We created a novel mutated form of human interleukin-13 (IL-13) in which a positively charged arg
106 nt protein-1 (MCP-1) and a later increase in interleukin-13 (IL-13) levels in the peritoneal cavity.
107 ates induced variable disease severity, lung interleukin-13 (IL-13) levels, and gob-5 levels in BALB/
108 h1) and Th2 cytokine mRNAs, we observed that interleukin-13 (IL-13) mRNA was highly expressed in HTLV
112 Ls also had high levels of expression of the interleukin-13 (IL-13) receptor and downstream effectors
115 T6 in KSHV-associated PEL cells results from interleukin-13 (IL-13) secretion and reduced expression
116 hat STAT6 activation tightly correlates with interleukin-13 (IL-13) secretion, JAK1/2 tyrosine phosph
117 te lymphoid cells (ILC2s) and their cytokine interleukin-13 (IL-13) signaled directly to inhibitory i
118 from wild-type BALB/c mice are polarized by interleukin-13 (IL-13) towards a tumor-promoting M2 phen
120 gh levels of the profibrotic type 2 cytokine interleukin-13 (IL-13) were produced following activatio
125 uired group 2 innate lymphoid cells (ILC2s), interleukin-13 (IL-13), and its receptor, IL-4Ra-IL-13Ra
126 ansforming growth factor-beta (TGF-beta) and interleukin-13 (IL-13), cytokines implicated in remodeli
127 ion and is associated with the production of interleukin-13 (IL-13), in resistance to this nematode.
128 Therefore, we tested the hypothesis that interleukin-13 (IL-13), which influences the differentia
129 thmatic airways, HAE cells were treated with interleukin-13 (IL-13), which reduced viral titers, vira
131 is induced via a T helper-2 (Th2)-specific, interleukin-13 (IL-13)-mediated pathway in epithelial ce
132 adoxically resulted in dramatic expansion of interleukin-13 (IL-13)-producing ILC2s and resistance to
136 crete mediators (including cytokines such as interleukin 13 [IL-13], IL-22, and oncostatin M) that ac
137 n type 2 T cells, we demonstrate that type 2 interleukin-13+ (IL-13+) T cells (CD4+ or CD8+) in human
138 those encoding human interleukin 4 (IL4) and interleukin 13 (IL13 ), which induce IgE class switching
141 ), interleukin 4 (Il4), interleukin 5 (Il5), interleukin 13 (Il13), and granulocyte-macrophage colony
142 se associated with increased serum levels of interleukin 13 (IL13), which might contribute to its pat
143 n in healthy tissue, motivating expansion of interleukin 13 (IL13)-based chimeric antigen receptor (C
149 nted that alpha-helices A, C, and D in human interleukin-13 (IL13) participate in interaction with it
151 o too have monoclonal antibodies targeted to interleukin 13 in patients with a type 2 allergic phenot
152 or necrosis factor alpha, interleukin 4, and interleukin 13 in the liver and spleen, which are associ
154 have revealed direct and distinct roles for interleukin-13 in fibrosis, steatosis, cholestasis, and
155 ecreased allergen-induced AHR, production of interleukin-13 in lung tissue, and lung eosinophilia.
157 a, goblet cell metaplasia, and expression of interleukin-13 in response to low-dose aerosolized aller
159 dy of lebrikizumab, a monoclonal antibody to interleukin-13, in 219 adults who had asthma that was in
160 ell immunity that involves interleukin-5 and interleukin-13-induced esophageal epithelial cell respon
162 d not, whereas antibodies to interleukin 10, interleukin 13, interferon alpha, or interferon gamma mo
163 evated production of interleukin 10 (IL-10), interleukin 13, interferon gamma, CXCL9, and CCL2 compar
164 leukin-10, interleukin-12/interleukin-23p40, interleukin-13, interleukin-17, interleukin-18, interfer
165 ory cytokines (interleukin-3, interleukin-6, interleukin-13, interleukin-17, macrophage inflammatory
166 interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory
168 cells from the actions of interleukin 4 and interleukin 13, is used as treatment for severe allergic
169 numab-a biological that specifically targets interleukin-13-is one of the newer advanced systemic tre
170 red receptor component for interleukin-4 and interleukin-13, key and central drivers of type 2 inflam
171 red receptor component for interleukin-4 and interleukin-13, key and central drivers of type 2 inflam
172 red receptor component for interleukin-4 and interleukin-13, key drivers of type 2 inflammation.
173 ortisol, AXL receptor kinase, interleukin-3, interleukin-13, matrix metalloproteinase-9 total, apolip
174 e by stimulating type 2 immunity, leading to interleukin-13-mediated epithelial and AMP expression ch
175 was observed to block the interleukin-4- or interleukin-13-mediated induction of CDw60 on cultured k
176 leukin-5, anti-interleukin-4Ralpha, and anti-interleukin-13 monoclonal antibodies in patients with se
177 In phase 2 trials, lebrikizumab, an anti-interleukin-13 monoclonal antibody, reduced exacerbation
179 d antibodies against IgE, interleukin 5, and interleukin 13, offer hope to improve the quality of lif
180 effect of the cytokines interferon-gamma and interleukin-13 or interleukin-4 on keratinocytes, alone
181 h those identified by microarray analysis of interleukin-13-overexpressing and integrin-beta6-deficie
182 the substantial local efficacy of BTZ-043 in interleukin-13-overexpressing mice, which mimic human TB
183 ogressive models of liver disease induced by interleukin-13 overexpression or after infection with Sc
184 ng early ART had higher day-14 CSF levels of interleukin-13 (P = .04), sCD14 (P = .04), sCD163 (P = .
188 lonal antibody that blocks interleukin-4 and interleukin-13 pathways and has shown efficacy in five d
189 oplatform, when subsequently conjugated with interleukin-13 peptide IL-13-Gd3N@C80(OH)x(NH2)y, exhibi
190 te that this agent can be conjugated with an interleukin-13 peptide that is designed to target an ove
191 -affinity IgG4 monoclonal antibody targeting interleukin-13, prevents the formation of the interleuki
192 macrophages stimulated with interleukin 4 + interleukin 13 produce arginase I, which decreases the e
193 ive immune response and is driven instead by interleukin-13 produced by macrophages that have been st
194 tly induces tuft cell expansion by promoting interleukin-13 production by innate lymphoid cells.
196 ore robust interleukin-4, interleukin-5, and interleukin-13 production than their mature naive counte
200 ubsets, but Th1 cells express high levels of interleukin 13 receptor alpha1 (IL-13R alpha 1), which h
202 olymorphonucleocyte (PMN) infiltration in an interleukin 13 receptor alpha2 (IL-13Ralpha2)-dependent
203 date intrathecal delivery of EPHA2, HER2 and interleukin 13 receptor alpha2 chimeric antigen receptor
204 three cell-surface targets, EPHA2, HER2 and interleukin 13 receptor alpha2, expressed on medulloblas
205 s, CCN proteins, fibroblast growth factor 2, interleukin 13 receptor components, proteases, antiprote
209 rowth factor receptor (EGFR) epitope 806 and interleukin-13 receptor alpha 2 (IL-13Ralpha2), or CART-
210 actor receptor (EGFR), EGFR variant III, and interleukin-13 receptor alpha 2 (IL13Ralpha2) on glioma
213 class II, beta(2)-microglobulin, clusterin, interleukin-13 receptor alpha chain, ovotransferrin, a s
216 r") platform into newly developed human anti-interleukin-13 receptor alpha-2 (IL13Ralpha2)-single-cel
217 Restricted and high-level expression of interleukin-13 receptor alpha2 (IL-13Ralpha2) in a major
221 lines have been reported to overexpress the interleukin-13 receptor alpha2 subunit (IL13Ralpha2) rel
222 ssion signature comprising a surface marker, interleukin-13 receptor subunit alpha 2 (IL13RA2), which
224 rcinoma (RCC) cells express large numbers of interleukin-13 receptors (IL-13R), a newly described hem
225 interleukin-13 as evidenced by the effect on interleukin-13-related pharmacodynamic biomarkers, and c
226 pwise progression (paligenosis) initiated by interleukin-13-secreting innate lymphoid cells (ILC2s).
230 onoclonal antibody, blocks interleukin-4 and interleukin-13 signaling, which have key roles in eosino
232 oclonal antibody, inhibits interleukin-4 and interleukin-13 signalling, key drivers of type-2-mediate
233 h2) response, or the pathogenic Th2 cytokine interleukin 13 significantly ameliorated pulmonary arter
234 have shown that the type 2 effector cytokine interleukin-13 simultaneously, yet independently, direct
235 eline (2.5-fold higher; p = 0.004) and after interleukin-13 stimulation (13-fold higher; p = 0.0001).
237 ts for EoE: anti-interleukin-5 therapy, anti-interleukin-13 therapy, anti-IgE therapy, montelukast, c
238 een in atopic asthma, with interleukin 4 and interleukin 13 thought to have a role in the physiologic
239 inhibiting the binding of interleukin 4 and interleukin 13 to interleukin-4Ralpha receptor complexes
240 terleukin-9, interleukin-10, interleukin-12, interleukin-13, tumor necrosis factor-alpha, interferon-
241 body) blocks signalling of interleukin 4 and interleukin 13, type 2/Th2 cytokines implicated in numer
242 ts secrete high levels of interleukin 10 and interleukin 13 upon in vitro restimulation, which are al
243 duction of CDw60 involving interleukin-4, or interleukin-13 was antagonized by interferon-gamma.
244 kin 1beta, interleukin 2, interleukin 6, and interleukin 13 were significantly greater in NW specimen
246 am regulators of the core network, including interleukin 13, which induced CM cell cycle entry and ST
247 complexes of the cytokines interleukin-4 and interleukin-13 with their receptors, showing how events
248 tion (chemokines CCL17, CCL18, and CCL26 and interleukin 13) with preferential activation of the JAK1