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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
31 e interleukin (IL) receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21.
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
33       Plasma interleukin (IL) 2, IL-4, IL-5, IL-7, IL-17, interferon-gamma, and tumor necrosis factor
34  DR-induced quiescence of HSCs, whereas IL-6/IL-7 substitutions rescued the impairment of B lymphopoi
35                               Interleukin 7 (IL-7) promotes the survival of TCRbeta(-) DN thymocytes
36 velopmental downregulation of interleukin 7 (IL-7)-receptor signaling in small pre-B cells induced ex
37 component of the receptor for interleukin-7 (IL-7) and the transcription factor c-myc.
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
40                               Interleukin-7 (IL-7) availability determines the size and proliferative
41                               Interleukin-7 (IL-7) engages multiple mechanisms to overcome chronic vi
42 ed by cytokines, particularly interleukin-7 (IL-7) for murine developing B cells.
43                  The cytokine interleukin-7 (IL-7) functions to enhance lymphocyte proliferation, sur
44 ts receiving suppressive ART, interleukin-7 (IL-7) increases the number of CD4(+) T cells by promotin
45                               Interleukin-7 (IL-7) is essential to T-cell survival as well as homeost
46                               Interleukin-7 (IL-7) is fundamental for thymopoiesis, T-cell homeostasi
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
51                     Exogenous Interleukin-7 (IL-7), in supplement to antiretroviral therapy, leads to
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.
56                                 Accordingly, IL-7-deficient DN4 cells lacked trophic receptors and di
57                                 In addition, IL-7 or thymic stromal lymphopoietin were able to replac
58                                 In addition, IL-7-stimulated pro-B cell cultures revealed a reduced d
59 s proliferation and did so without affecting IL-7 levels.
60 r than 70 days in the lung and airways in an IL-7 dependent fashion.
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
64                             IL-2, IL-15, and IL-7 are collectively dispensable for 4-1BB expression o
65                  We found that IL-1alpha and IL-7 secreted from keratinocytes work in tandem to expan
66  by low levels of the interleukin (IL)-2 and IL-7 receptors (CD25(-)CD127(-)).
67 al interleukin receptors, including IL-2 and IL-7 receptors.
68 IL-8, IL-10, fibroblast growth factor 2, and IL-7 remained higher.
69 address the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics durin
70 rvivors (P < 0.05 for all), whereas IL-4 and IL-7 were lower (P < 0.05).
71                         High plasma IL-5 and IL-7 levels pre-ART were associated with increased risk
72 red to controls (all P < .05), with IL-5 and IL-7 significant after Bonferroni-Holm correction.
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:
78 e interplay between IFN-gamma/IFN-gammaR and IL-7/IL-7R pathways.
79 is a cause of the T cell hyperactivation and IL-7 signaling pathway defects that are observed in some
80 th increased surface expression of c-Kit and IL-7 receptors on the IL-18-treated cells.
81 resumably via interaction with the c-Kit and IL-7 signaling axis.
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.
85 L-4, renders DCs responsive to both TSLP and IL-7.
86      Thymic stromal lymphopoietin (TSLP) and IL-7 are related cytokines that mediate growth and diffe
87 complex, a heterodimer composed of TSLPR and IL-7 receptor alpha (CD127).
88                            In vivo IL-7/anti-IL-7 mAb complexes selectively expanded and enhanced the
89 reaction and developed non-neutralizing anti-IL-7 antibodies.
90         We found that a short course of anti-IL-7 receptor blocking antibody following T cell depleti
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
96                                      Because IL-7 was shown to interfere with T cell functionality, w
97 herapy relies on the interdependence between IL-7 and IFN-gamma signalling in T cells, as lack of eit
98                                     Blocking IL-7 signaling reduced the Th17 autoimmune compartment b
99       Here, we investigated whether blocking IL-7 signaling with a mAb that targets IL-7 receptor alp
100           PLCgamma pathway inhibition blocks IL-7-induced activation of mTOR, but not Stat5.
101 meostatic proliferation, partially driven by IL-7, continues to replenish tolerance-refractory immune
102 transplantation and appeared to be driven by IL-7-mediated homeostatic T cell proliferation.
103 lls before antigen recognition is ensured by IL-7, which drives expression of the prosurvival factor
104  CD25(-) naive CD4 T cells can be induced by IL-7 in vitro in the absence of TCR activation.
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
108 recursors failed to undergo a characteristic IL-7-dependent proliferative burst.
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
111            Because the lymphotropic cytokine IL-7 plays crucial roles in both development of TN in th
112                                 The cytokine IL-7 is important for controlling lymphopoiesis under bo
113 optosis in response to homeostatic cytokines IL-7 and IL-15.
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
117 ded on the presence of hair follicle-derived IL-7.
118                However, whether host-derived IL-7 plays a role in driving the proper function of CD4+
119 hat CD4(+)CD3(-) innate-like T cells display IL-7-dependent induction of surface lymphotoxin-alphabet
120 l development does not result from disrupted IL-7 signaling.
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.
123 m depleted patients showed markedly elevated IL-7 levels posttransplantation.
124 ing their IL-7 receptor expression, enabling IL-7 to sustain them as memory T cells.
125  to increased availability of the endogenous IL-7 in mice.
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
129                       Serum was analyzed for IL-7.
130  of clinical data revealed the potential for IL-7 to achieve sustained CD4+ T cell restoration with l
131          These data support a novel role for IL-7 in the repression of the TFH gene program and evoke
132 hile conditional Cxcl12 or Scf deletion from IL-7(+) cells reduced HSC and MPP numbers.
133                                 Furthermore, IL-7 inhibition in combination with T cell depletion syn
134 tein [MIP]-1alpha, MIP-1beta), hematopoietic IL-7, and granulocyte macrophage colony-stimulating fact
135                            Importantly, high IL-7 expression was detected in the CNS during EAE and c
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
139  metabolism in sepsis with recombinant human IL-7 as a treatment option.
140 d the beneficial effect of recombinant human IL-7.
141 PLCgamma/PKC-induced mTOR activation impairs IL-7-mediated B cell development.
142 ient mice overexpressing Bcl2, as well as in IL-7 transgenic mice suggests that both FL and IL-7 regu
143 sion of PDPN resulted in profound defects in IL-7-mediated T cell expansion and survival.
144       These data suggest that differences in IL-7-dependent proliferation is one exploitable mechanis
145         CD3/28-activated T cells expanded in IL-7 and IL-15 produced greater expansion of memory stem
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
151 in gut immunity and tissue repair, including IL-7, Ccl2, Ptgs2, and Amphiregulin.
152 mentally cued regulatory signaling including IL-7/STAT5 and cellular events such as immunoglobulin re
153                                    Increased IL-7 availability enhanced Treg survival, stabilized Tre
154               C. rodentium infection induced IL-7 production from intestinal epithelial cells (IECs).
155 f CD45 on innate immune cells in influencing IL-7 production by lymphoid stromal cells.
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
158                      However, despite intact IL-7 signaling, GON4L-deficient pro-B cell stage precurs
159                                Intriguingly, IL-7 diminished the suppressive activity of DN T cells t
160  rescue of B-cell commitment in mice lacking IL-7 but simultaneously overexpressing FL.
161 T cells, and prevent early and increase late IL-7 induction by lymph node stromal cells.
162 gamma-chain (gammac) receptor but that, like IL-7 and IL-15, induced expression of the lineage-specif
163 of other homeostatic regulators, most likely IL-7.
164 stained CD4+ T cell restoration with limited IL-7 exposure in HIV-1 infected patients with immune fai
165 L-7, were primarily responsible for limiting IL-7 availability via their expression of IL-7R.
166 pression of genes related to B cell lineage, IL-7 signaling, and cell cycle.
167 induced homeostatic proliferation to measure IL-7 availability in vivo, we found that radioresistant
168                             Mechanistically, IL-7-dependent activation of STAT5 contributes to Bcl-6
169  Our studies indicate that endogenous murine IL-7 is part of the normal host response to Pneumocystis
170 a novel rabies vaccine that expressed murine IL-7 was developed.
171 sthmatic patients had increased TSLP but not IL-7 levels.
172 ly thymic development by genetic ablation of IL-7 receptoralpha or Hes1.
173                Conversely, in the absence of IL-7 and stem cell factor, cNK cells were generated but
174  self-renewal of DN4 cells in the absence of IL-7, but overexpression of BCL2 did not.
175 he several potential mechanisms of action of IL-7 is unknown.
176                    Nevertheless, addition of IL-7 enhanced pre-B cell expansion and inhibited maturat
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
180 least in part, to additional availability of IL-7.
181 ption and, thus, enhances the bioactivity of IL-7 when the cytokine is limited, as it is presumed to
182 ecific CD8 T cells 10 wk after completion of IL-7 treatment.
183 that TAG synthesis is a central component of IL-7-mediated survival of human and mouse memory CD8+T c
184 nd ERK pathways at similar concentrations of IL-7 detected in RA synovial fluid.
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
187 ls by inhibiting the proliferative effect of IL-7.
188  naive T cells to the prosurvival effects of IL-7 and allowing T-cell persistence in vivo.
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
193 urvival molecule Bcl-2, but the functions of IL-7 during beta-selection have remained unclear.
194 , and appeared to be limited by induction of IL-7 nonresponsiveness.
195                          The serum levels of IL-7 were also increased in chronic chagasic patients.
196 owing culture with IFN-alpha8, and levels of IL-7-induced phosphorylated STAT5 were increased by IFN-
197 c stromal lymphopoietin (TSLP), 2 ligands of IL-7 receptor alpha.
198 ata suggest that a compensatory mechanism of IL-7-mediated homeostatic proliferation can restore the
199                      Despite of a paucity of IL-7 in the immune milieu, CTX preconditioning allowed a
200 1c(+) cells and the second the production of IL-7 by lymphoid stromal cells.
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
205                 Here we assessed the role of IL-7, a key cytokine regulating T-cell homeostasis, in s
206                             Sequestration of IL-7 or impairment of IL-7R signaling after allograft tr
207 that radioresistant cells were the source of IL-7 for both CD4(+) and CD8(+) T cells.
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
211  The first wave of expansion is dependent on IL-7.
212 lls were found to have a potent influence on IL-7 amounts in the primary and secondary lymphoid tissu
213 t that PU.1 and Spi-B activate Btk to oppose IL-7 responsiveness in developing B cells.
214 nterleukin-7(+) (IL-7) cells and for optimal IL-7 receptor signaling.
215 mulation with IL-2 or IL-15, but not IL-4 or IL-7.
216 s in the presence or absence of IL-18 and/or IL-7.
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
219       The present study highlights perturbed IL-7/IL-7R T cell signaling through STAT5 as a potential
220         Treg cells can control physiological IL-7 production that is indispensable for normal B-cell
221                                 IEC-produced IL-7 was only essential for protective immunity against
222 on) but inhibited homeostatic proliferation (IL-7 induced) of CD4(+) and CD8(+) T cells.
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
225  and highlight the usefulness of recombinant IL-7 as an adjuvant for adoptive immunotherapy.
226 ndicate that the ability of cells to recycle IL-7 is dependent on IL-7R alpha-chain (CD127) and endoc
227 absence of intracellular TCRbeta and reduced IL-7 signaling.
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
230 y communicate with stromal cells to regulate IL-7 production.
231                                       rLBNSE-IL-7 induced higher rates of T follicular helper (Tfh) c
232 rleukin-7 (IL-7), referred to here as rLBNSE-IL-7, was constructed, and its effectiveness was evaluat
233                        Interestingly, rLBNSE-IL-7 improved the percentages of long-lived memory B cel
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
238 r, the mechanisms that regulate steady-state IL-7 amounts are unclear.
239                           sgammac suppressed IL-7 signaling to impair naive T cell survival during ho
240 cking IL-7 signaling with a mAb that targets IL-7 receptor alpha (IL-7Ralpha) alone or following T ce
241               These results demonstrate that IL-7 homeostasis is achieved through consumption by mult
242    Collectively, these data demonstrate that IL-7 is produced by IECs in response to C. rodentium inf
243              Furthermore, we determined that IL-7 signaling is important for the homeostasis of these
244                             We discover that IL-7 induces expression of the glycerol channel aquapori
245    In this article, we provide evidence that IL-7 utilization is enhanced by a novel mechanism of cyt
246                           Here we found that IL-7 signaled TCRbeta(+) DN3 and DN4 thymocytes to upreg
247                 These findings indicate that IL-7 and Akt/mTOR signaling are critical factors for the
248 -cell progenitors, therefore indicating that IL-7 can be dispensable for commitment to the B-cell lin
249       Of interest, our studies revealed that IL-7 activates the Akt/mechanistic target of rapamycin (
250                            Here we show that IL-7 receptor (IL-7R) is not strictly required for the d
251                In this article, we show that IL-7 therapy in humans increases the number of circulati
252                 Previous results showed that IL-7 can restore TRAF1 expression in virus-specific CD8
253 ions into the involved mechanism showed that IL-7 is a novel and potent chemoattractant that attracts
254                          We also showed that IL-7-induced bone loss in vivo is associated with Th17 c
255                                          The IL-7/IL-7R signaling axis participates in cell survival,
256 1), recent thymic emigration (CD31), and the IL-7 receptor-alpha (IL-7Ralpha).
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
260            Further analyses suggest that the IL-7/Akt/mTOR signaling cascade downregulates anergy-ass
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
263 g a lack of homeostatic cell control through IL-7 signalling.
264                                        Thus, IL-7 critically acts cooperatively with signaling via th
265                                        Thus, IL-7 receptor controls early B lymphopoiesis through act
266                                        Thus, IL-7 therapy in antiretroviral therapy-treated patients
267 e-negative 3 stage, similar in efficiency to IL-7.
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
273 and is associated with impaired responses to IL-7.
274 ent RORgammat(+) ILCs are less responsive to IL-7 mediated signalling, more prone to apoptosis and pr
275 27(high) subset that is highly responsive to IL-7.
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
279 ory T-cell development and responsiveness to IL-7-dependent signals.
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
282 n encounter by controlling susceptibility to IL-7.
283 d renders B cell progenitors unresponsive to IL-7.
284 re and the first year after transplantation, IL-7 and IL-2 induced STAT5 phosphorylation, and the exp
285 echanism that enables cells to optimally use IL-7.
286                                      In vivo IL-7/anti-IL-7 mAb complexes selectively expanded and en
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
289 omain, repressed Btla transcription, whereas IL-7 increased BTLA levels on the cell surface.
290 endocytosis, consistent with a model whereby IL-7 is internalized via receptor interactions before re
291  with T cell functionality, we asked whether IL-7 affects the functionality of human DN T cells.
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
298 bility, further enhanced by stimulation with IL-7.
299                    IL-18 showed synergy with IL-7 and enhanced proliferation of both the thymus-deriv
300                               Treatment with IL-7/mAb complexes can restore naive T cell homeostatic

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