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1 IL-7 administration in vivo failed to boost B cell devel
2 IL-7 and IL-18 act synergistically to upregulate express
3 IL-7 and TSLP abrogated this inhibition and induced ster
4 IL-7 increases total circulating CD4 and CD8 T cell coun
5 IL-7 inhibited the differentiation of Th17 cells, but pr
6 IL-7 is a key homeostatic cytokine that provides signals
7 IL-7 is critical for murine T and B cell development and
8 IL-7 is one such cytokine capable of augmenting the func
9 IL-7 production from IECs in response to C. rodentium wa
10 IL-7 receptor alpha (IL-7Ralpha) expression is subject t
11 IL-7 therapy did not reduce TCR diversity of the memory
12 IL-7 therapy has been evaluated in patients who do not r
13 IL-7 treatment improved mTOR activation, GLUT1 expressio
14 IL-7 treatment increased levels of phospho-ribosomal pro
15 IL-7(+) cells expressed CXCL12 and the cytokine SCF, wer
16 IL-7, IL-22, GM-CSF, and CCL2 were resistant to chymase
17 IL-7-induced phosphorylation of STAT5 as well as Bcl-2 a
18 BOS IL-1beta (P<0.001), IL-1Ralpha (P<0.01), IL-7 (P<0.05), IL-8/CXCL8 (P<0.001), MCP-3/CXCCL7 (P<0.0
19 nterleukin (IL)-4 (P = .02), IL-6 (P = .01), IL-7 (P = .04), IL-8 (P = .03), and interferon gamma (P
20 nude recipients and NK cells in E4BP4/Rag-1/IL-7 triple-KO mice indicated thymus-independent NK cell
21 IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10, IL-7, IL-1alpha, and IL-5) subject-to-subject variation.
22 homeostatic cytokines interleukin-2 (IL-2), IL-7, and IL-15 can induce CD4 downregulation in vitro.
23 in vitro by anti-CD3, interleukin-2 (IL-2), IL-7, or IL-15 but not by Toll-like receptor ligands.
24 -4, IL-9, IL-10, fibroblast growth factor 2, IL-7, IL-15, and transforming growth factor alpha) but l
25 Finally, we show that the cytokines IL-2, IL-7, and IL-15, which induce homeostatic T cell prolife
26 ious cytokines known to activate ILCs (IL-2, IL-7, IL-12, thymic stromal lymphopoietin (TSLP), IL-25,
27 ls, whereas exposure of CD8 T cells to IL-2, IL-7, IL-15, and IL-21 increased granzyme B production.
28 T cell counts but not to the levels of IL-2, IL-7, or IL-15, while in HIV-negative donors, memory CD4
29 n metabolites inhibited interleukin (IL)-2-, IL-7-, and IL-15-dependent expansion of CARTs; diminishe
30 icellulose, xylose value was high in IL 6-3, IL 7-2 and IL 6-2, whereas arabinose showed a low conten
32 pha), CXCL10 (IP-10), IFN-gamma, IL-4, IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LI
34 DR-induced quiescence of HSCs, whereas IL-6/IL-7 substitutions rescued the impairment of B lymphopoi
36 velopmental downregulation of interleukin 7 (IL-7)-receptor signaling in small pre-B cells induced ex
38 rt mutations in receptors for interleukin-7 (IL-7) and thymic stromal lymphopoietin (TSLP), resulting
39 nase-3 (Flt3) ligand (FL) and Interleukin-7 (IL-7) are cytokines pivotal for B-cell development, as m
44 ts receiving suppressive ART, interleukin-7 (IL-7) increases the number of CD4(+) T cells by promotin
47 feration of infected cells by interleukin-7 (IL-7) or antigenic stimulation, as well as new rounds of
48 aused a downregulation of the interleukin-7 (IL-7) receptor, needed for survival of conventional T ce
49 ainst reinfection and require interleukin-7 (IL-7), but the mechanisms by which IL-7 controls memory
50 engagement in the presence of interleukin-7 (IL-7), IL-21, and the glycogen synthase-3beta inhibitor
52 (RABV) that expressed murine interleukin-7 (IL-7), referred to here as rLBNSE-IL-7, was constructed,
53 ain cytokines (CGCC), such as interleukin-7 (IL-7), render resting CD4 T cells permissible to HIV-1 i
54 iple hematopoietic cytokines (interleukin-7 [IL-7], Flt3L, stem cell factor [SCF], ThPO, and IL-6) fr
55 d for CLP positioning near Interleukin-7(+) (IL-7) cells and for optimal IL-7 receptor signaling.
61 deficient T cells survived far longer, in an IL-7-dependent manner, but failed to undergo lymphopenia
62 ence interval {CI}, .77-43.0]; P = .088) and IL-7 (HR, 9.30 [95% CI, 1.96-44.0]; P = .005) were predi
63 nd a novel mechanism through which IL-12 and IL-7 synergistically control granzyme B through upregula
69 address the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics durin
73 ); interferon gamma, interleukin (IL)-6, and IL-7 in CC group compared to Ctrl; and IL-8 in both UC a
74 en-binding integrin alpha2beta1 (CD49b), and IL-7 increases their adhesion to collagen via alpha2beta
75 between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previously been proposed, but h
76 IL-15 was required for CD8(+) TRM cells, and IL-7 for CD8(+) and CD4(+) TRM cells, to exert epidermot
77 -7 transgenic mice suggests that both FL and IL-7 regulate B-cell commitment in a permissive manner:
79 is a cause of the T cell hyperactivation and IL-7 signaling pathway defects that are observed in some
82 ng experimental lymphopenic mouse models and IL-7-induced homeostatic proliferation to measure IL-7 a
83 6D(+)CD135(+)CD127(+)CD19(-) progenitors and IL-7 by providing survival signals to these progenitors.
84 eplication stress by integrating pre-TCR and IL-7 signaling with DNA damage and cell cycle control.
91 Importantly, we found that cytokines such as IL-7 and IL-4, which are particularly active in sites of
92 ith heterodimeric cytokine receptors such as IL-7 receptor or IL-9 receptor, in which JAK1 is appende
93 ly, sIL7Ralpha competes with cell-associated IL-7 receptor to diminish excessive IL-7 consumption and
94 cells (PBMCs) to IL-6 or IL-1beta attenuates IL-7-induced Stat5 phosphorylation and induction of the
95 pro-B progenitor homeostasis by attenuating IL-7-stimuated JAK/STAT5 signaling via a direct interact
97 herapy relies on the interdependence between IL-7 and IFN-gamma signalling in T cells, as lack of eit
101 meostatic proliferation, partially driven by IL-7, continues to replenish tolerance-refractory immune
103 lls before antigen recognition is ensured by IL-7, which drives expression of the prosurvival factor
105 We propose that synergistic sensitization by IL-7 and IL-18 to self-peptide ligand may represent a no
106 dant to its role in suppressing signaling by IL-7, a critical gammac cytokine in early thymopoiesis.
107 HGF), T-cell development/activation (CD40L, IL-7, CCL25, IL-2RB, IL-15RA, CD6) and angiogenesis (VEG
109 plantation and other lymphopenic conditions, IL-7 plays an important role in the reconstitution, surv
110 of FRC-derived chemokine CCL21 and cytokine IL-7 were accompanied by altered composition and aberran
114 cal trials include KGF, use of the cytokines IL-7 and IL-22, and hormonal modulation including growth
115 -stimulating factor) and adaptive cytokines (IL-7 and IL-15) and higher frequencies of activated T ce
116 clude keratinocyte growth factor, cytokines (IL-7 and IL-22), and hormonal modulation including sex s
119 hat CD4(+)CD3(-) innate-like T cells display IL-7-dependent induction of surface lymphotoxin-alphabet
121 vo, and that IL-18 synergizes with high-dose IL-7 in a TRAF6-dependent manner to induce slow, LIP/hom
122 demethylation was heritably preserved during IL-7- and IL-15-mediated in vitro cell proliferation.
126 suggest caution in relying on the endogenous IL-7 to enhance donor T cell expansion and persistence a
127 ) on CD4(+) and CD8(+) T cells and evaluated IL-7-dependent signaling events in patients at different
128 sociated IL-7 receptor to diminish excessive IL-7 consumption and, thus, enhances the bioactivity of
130 of clinical data revealed the potential for IL-7 to achieve sustained CD4+ T cell restoration with l
134 tein [MIP]-1alpha, MIP-1beta), hematopoietic IL-7, and granulocyte macrophage colony-stimulating fact
136 impaired clearance of cryptococci while high IL-7 levels may reflect IL-7/IL-7R pathway dysfunction i
137 of 3 subcutaneous doses of recombinant human IL-7 (rhIL-7) per week in patients with ICL who were at
138 esized that treatment with recombinant human IL-7 (rhIL-7) would augment host defense against Pneumoc
142 ient mice overexpressing Bcl2, as well as in IL-7 transgenic mice suggests that both FL and IL-7 regu
146 ha Tyr(449) cytoplasmic SH2-binding motif in IL-7-mediated B cell development using a knock-in mouse
147 in T-cell development caused by mutations in IL-7 receptor alpha (IL7RA) and IL-2 receptor gamma (IL2
148 tained demonstrate that FL overexpression in IL-7-deficient mice rescues B-cell commitment, resulting
149 y6D(+)CD135(+)CD127(+)CD19(-) progenitors in IL-7- or FL-deficient mice overexpressing Bcl2, as well
150 The defect was not due to a reduction in IL-7 expression, but from a combination of changes in th
152 mentally cued regulatory signaling including IL-7/STAT5 and cellular events such as immunoglobulin re
156 SOCS family activity consequently inhibited IL-7-mediated STAT5 activation and T cell homeostatic pr
157 1 integrin with a neutralizing mAb inhibited IL-7-induced bone loss and osteoclast numbers by reducin
162 gamma-chain (gammac) receptor but that, like IL-7 and IL-15, induced expression of the lineage-specif
164 stained CD4+ T cell restoration with limited IL-7 exposure in HIV-1 infected patients with immune fai
167 induced homeostatic proliferation to measure IL-7 availability in vivo, we found that radioresistant
169 Our studies indicate that endogenous murine IL-7 is part of the normal host response to Pneumocystis
177 xtent to which therapeutic administration of IL-7 could reverse TN deficiency in aging rhesus macaque
178 maintained during repeated administration of IL-7, our simulation study shows that such a strategy ma
179 n enhanced cell cycle entry and apoptosis of IL-7-dependent pro-B cells, blocking Ig synthesis and B
181 ption and, thus, enhances the bioactivity of IL-7 when the cytokine is limited, as it is presumed to
183 that TAG synthesis is a central component of IL-7-mediated survival of human and mouse memory CD8+T c
185 ne marrow as well as serum concentrations of IL-7, Flt3L, SCF, and ThPO to the levels displayed by sp
186 itizes Treg cell to the biological effect of IL-7, possibly rendering more common gammac-chain availa
189 trials that exploit the mitogenic effects of IL-7 have achieved success in treating human diseases.
190 strated that the immune-enhancing effects of IL-7 were also applicable to donor CD4+ T cells pre-acti
191 These results suggest that the expression of IL-7 is beneficial for induction of potent and long-last
192 dexamethasone upregulated ILC2 expression of IL-7 receptor alpha, which augmented and sustained signa
196 owing culture with IFN-alpha8, and levels of IL-7-induced phosphorylated STAT5 were increased by IFN-
198 ata suggest that a compensatory mechanism of IL-7-mediated homeostatic proliferation can restore the
201 rosine kinase (BTK), a negative regulator of IL-7 signaling, was reduced in preleukemic and leukemic
202 me chronic viral infections, but the role of IL-7 in bacterial infections, especially enteric bacteri
203 ver, there is little known about the role of IL-7 in PCP or its potential use as an immunotherapeutic
204 racterized the previously unexplored role of IL-7 in the innate immune response to the attaching and
208 ge cells, although irrelevant as a source of IL-7, were primarily responsible for limiting IL-7 avail
209 ys an important role in the transcription of IL-7 receptor alpha-subunit (CD127), enabling responsive
210 ence, the inhibitory effects of IFN-alpha on IL-7-induced proliferation of CD4(+) T cells are unlikel
212 lls were found to have a potent influence on IL-7 amounts in the primary and secondary lymphoid tissu
217 for 7 d with staphylococcal enterotoxin B or IL-7 in the absence or presence of 100 U/ml IFN-alpha8.
218 verall, our data suggest that overexpressing IL-7 improved the induction of long-lasting primary and
223 nsient increase of peripheral proliferation, IL-7 exerts additional effects that play a significant r
224 ly, supplementation of exogenous recombinant IL-7 markedly amplified and sustained polyfunctional CD4
226 ndicate that the ability of cells to recycle IL-7 is dependent on IL-7R alpha-chain (CD127) and endoc
228 The absence of CD45 also led to reduced IL-7 production by lymphoid stromal cells, suggesting an
229 yptococci while high IL-7 levels may reflect IL-7/IL-7R pathway dysfunction in T cells, both of which
232 rleukin-7 (IL-7), referred to here as rLBNSE-IL-7, was constructed, and its effectiveness was evaluat
234 em and PCs after a boost with rLBNSE, rLBNSE-IL-7-immunized mice promptly produced a more potent seco
235 he IL-7-expressing recombinant virus (rLBNSE-IL-7) were able to sustain VNA levels much longer than t
236 higher numbers for up to 360 dpi with rLBNSE-IL-7 compared to rLBNSE, could differentiate into antibo
237 ) and old (>20 y) RM with recombinant simian IL-7 (rsIL-7) results in only transient increases in per
240 cking IL-7 signaling with a mAb that targets IL-7 receptor alpha (IL-7Ralpha) alone or following T ce
242 Collectively, these data demonstrate that IL-7 is produced by IECs in response to C. rodentium inf
245 In this article, we provide evidence that IL-7 utilization is enhanced by a novel mechanism of cyt
248 -cell progenitors, therefore indicating that IL-7 can be dispensable for commitment to the B-cell lin
253 ions into the involved mechanism showed that IL-7 is a novel and potent chemoattractant that attracts
257 ified the silencing of the IL7R gene and the IL-7 signaling pathway genes as potential biomarkers.
258 the long-lived PCs that were elicited by the IL-7-expressing recombinant virus (rLBNSE-IL-7) were abl
259 the protein kinases Akt or mTOR reversed the IL-7 effect, thereby restoring the functionality of DN T
261 D4+, and CD8+ T cells were affected in their IL-7-dependent phosphorylation of STAT5 (pSTAT5) which w
262 cells and by permanently upregulating their IL-7 receptor expression, enabling IL-7 to sustain them
268 -/- pro-B progenitors were hypersensitive to IL-7, exhibited marked self-renewal in vitro and in vivo
269 -deficient pro-B cells are hyporesponsive to IL-7, a key cytokine required for early B cell developme
270 s, memory CD4+ T cell cycling was related to IL-7 levels and negatively related to the plasma levels
271 ble degradation of Socs mRNAs in response to IL-7 signalling in order to reprogram naive T cells for
272 nstrated robust proliferation in response to IL-7, whereas more differentiated cells proliferated poo
274 ent RORgammat(+) ILCs are less responsive to IL-7 mediated signalling, more prone to apoptosis and pr
276 DeltaPB mice had increased responsiveness to IL-7 and could proliferate indefinitely in response to t
277 over and diminished T-cell responsiveness to IL-7 by IL-1beta and IL-6 exposure may contribute to the
278 7R and concomitant limited responsiveness to IL-7 signals as a common mechanism resulting in reduced
280 regain IL-7Ralpha expression, giving rise to IL-7-responsive polyfunctional CD4+ effector cells.
281 n, TEM became increasingly more sensitive to IL-7 stimulation in vivo, and transcriptional analysis o
284 re and the first year after transplantation, IL-7 and IL-2 induced STAT5 phosphorylation, and the exp
287 cell development in HNF1A(-/-) mice, whereas IL-7 stimulation of HNF1A(-/-) B cell progenitors in vit
288 o IL-6 favours the TFH gene program, whereas IL-7 signalling represses TFH-associated genes including
290 endocytosis, consistent with a model whereby IL-7 is internalized via receptor interactions before re
292 leukin-7 (IL-7), but the mechanisms by which IL-7 controls memory T cell survival, particularly metab
293 y uncovers the metabolic mechanisms by which IL-7 tailors the metabolism of memory T cells to promote
294 at combining immune checkpoint blockade with IL-7 signalling could be an effective modality to improv
295 the infused line by culturing the cells with IL-7 and IL-15 produced greater antitumor activity of CA
296 ecause TSLP shares signaling components with IL-7, a cytokine important for the development and survi
297 id not do so when ILC2s were stimulated with IL-7 and thymic stromal lymphopoietin (TSLP), 2 ligands
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