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1 IL-2R signaling influences two discrete aspects of immun
2 IL-2R signaling was also important for CD8(+) T cell imm
3 IL-2R signaling was indispensable for T(reg) cell homeos
4 IL-2R stimulation results in a G(1) cell cycle arrest, c
5 IL-2R typically was detected on less than 10% of lymphoc
6 IL-2R-derived signals are also required for their matura
7 = 90), increased levels of IL-8 (P < .001), IL-2R (P < .001), IL-12 (P < .001), IL-15 (P = .001), an
9 reased interleukin-1beta (IL-1beta), IL-1RA, IL-2R, IL-6, IL-8, IL-10, IL-12, IL-13, IL-15, tumor nec
13 inhibitors impaired internalization of IL-2.IL-2R and prevented the lysosomal degradation of this cy
15 onsistent with a stepwise assembly from IL-2/IL-2R alpha to IL-2/IL-2R alpha/IL-2R beta to IL-2/IL-2R
16 pwise assembly from IL-2/IL-2R alpha to IL-2/IL-2R alpha/IL-2R beta to IL-2/IL-2R alpha/IL-2R beta/ga
18 not appear to be a direct role for the IL-2/IL-2R autocrine pathway within the microenvironment of t
20 activates Tregs to broadly induce their IL-2/IL-2R gene program and provide a molecular underpinning
21 D4+CD25+ T(reg) cells, we show that the IL-2/IL-2R interaction is active in the thymus at the earlies
23 l, we investigated the possibility that IL-2/IL-2R interactions contribute to the deletion of self-re
24 Furthermore, disruption or blockade of IL-2/IL-2R interactions in vivo during Ag-mediated selection
25 subunit forms the largest of the three IL-2/IL-2R interfaces, which, together with the high abundanc
27 dence for the direct involvement of the IL-2/IL-2R signaling pathway in the deletion of Ag-specific t
29 cate that the essential function of the IL-2/IL-2R system primarily lies at the level of the producti
30 This augments the activation of the IL-2/IL-2R/STAT5 pathway and enhances cell proliferation in r
31 thymocytes up-regulate expression of IL-2RS: IL-2R(+) double-positive and CD4 single-positive thymocy
32 tic value of these five cytokines, and IL-8, IL-2R, IL-12, and IL-15 remained significant when risk s
36 T cells failed to express the high affinity IL-2R (CD25) while proliferating in vivo, irrespective o
40 racterized by up-regulation of high affinity IL-2R, but a failure to produce IL-2, and uncoupling of
41 egulatory T cells up-regulated high affinity IL-2R, but failed to produce IL-2, express cyclins or c-
42 process using mAbs against the high affinity IL-2R, CD25, and IL-2 in prolonging skin allograft survi
43 IL-15, which does not use the high affinity IL-2R, completely restored the ability of T cells to pho
45 2-mediated upregulation of the high-affinity IL-2R (CD25) and a subsequent increase in the sensitivit
51 te that the regulatory role of high-affinity IL-2R signals extends beyond the control of Ag-specific
52 ction of IL-2 and induction of high-affinity IL-2R upon TCR engagement has precluded a clear distinct
54 ion of the other chains of the high-affinity IL-2R, indicating an autonomous and previously unappreci
56 on of CD25, a component of the high-affinity IL-2R, was also reduced in response to IL-2 or after in
59 titutively express the intermediate-affinity IL-2R (beta-gamma dimers) and play a critical role in an
60 T(M) cells through its abundant low-affinity IL-2R, resulting in systemic CD8(+) T(M) cell dominance.
66 he IL-2R pathway and suggest that an altered IL-2R signaling signature may be a biomarker for type 1
69 re we show that up-regulation of Bcl-2 by an IL-2R lacking IL-2Rbeta tyrosine residues leads to incre
71 s on CIA using transgenic mice expressing an IL-2R beta/IL-4R alpha chimeric cytokine receptor transg
73 G patients were combined in a meta-analysis, IL-2R, IL-1RA, and CXCL9 (P = .013, .042, and .0012) wer
74 e colony-stimulating factor, IL-1Ralpha, and IL-2R were serially analyzed in 31 BOS+ and matched 31 B
77 During this phase, signals from CD28 and IL-2R cooperate with the TCR to "tune" this threshold by
79 y reduced the day-14 percentages of CD3+ and IL-2R+ cells in allogeneic BMT mice, producing results s
80 ns cells at 6 days after infection, CD4+ and IL-2R+ T cells at 5 days after infection, enhanced DTH,
81 TCR-mediated intracellular calcium flux and IL-2R-coupled STAT5 activation remain intact in these ce
82 mab, IL-2 serum concentrations increased and IL-2R bg signaling induced STAT5 phosphorylation and sus
83 Effects of MV on signaling via the TCR and IL-2R and proliferation or apoptosis of activated primar
86 mmunosuppression regimen (rapamycin and anti-IL-2R monoclonal antibody [mAb]) or the base immunosuppr
88 Animals receiving the LEA29Y/rapamycin/anti-IL-2R regimen (n = 5) had significantly prolonged islet
93 Furthermore, induction treatment with anti-IL-2R mAb did not prevent the development of these regul
94 dependent, the GMIL2R delivers an augmented IL-2R signal exclusively to CD8(+) T cells responding to
95 examined the effect of delivering augmented IL-2R signals selectively to CD8(+) T cells responding t
97 s capable of augmented, regulated, autocrine IL-2R signaling after target recognition by means of exp
98 CD8+ memory T cells lacking the high-avidity IL-2R results in a failure to repopulate the effector po
100 e previously reported an association between IL-2R mutations and susceptibility to visceral leishmani
102 , our findings provide a direct link between IL-2R subunit signaling and Ets1 expression and helps to
107 the activation of the NF-kappa B pathway by IL-2R signals in NK cells involves activation of the IKK
108 e some of the parallel pathways triggered by IL-2R signaling are sensitive to the effects of rapamyci
111 raft function were treated with either SRL/c-IL-2R mAb/prednisone (Pred) with inception of cyclospori
114 okines within the IL-2 receptor gamma chain (IL-2R gamma) superfamily that possess similar and unique
117 way sequentially linking CD28 costimulation, IL-2R signaling, and mTOR activation as important requir
120 unization protocol with transiently enhanced IL-2R signaling in normal mice led to persistent polyclo
121 s issue, we examined the effect of enhancing IL-2R signals in CD8(+) T cells after antigen stimulatio
122 dritic cells (hDCs) produce IL-2 and express IL-2R alpha-chain (CD25), but the role of IL-2 in DC fun
124 mphoma is that very few normal cells express IL-2R alpha, whereas the abnormal T cells in patients wi
128 s cellular system revealed a requirement for IL-2R expression for CD40 ligand-initiated, IL-12-driven
133 we report that administration of a humanized IL-2R blocking Ab induced a 4- to 20-fold expansion of C
139 -mediated protection, CIA was exacerbated in IL-2R beta/IL-4R alpha chimeric receptor transgenic mice
141 In contrast, CD28 engagement also increases IL-2R surface expression, but the up-regulation does not
142 elective blocking of PDE4 activity inhibited IL-2R expression and thereby led to abolishing HIV-1 DNA
144 tinib (CP-690,550) and the anti-interleukin (IL)-2R antibody basiliximab, as part of a phase 2 study.
145 fector); the cytokine receptors interleukin (IL)-2R beta , common gamma (C gamma ) chain, IL-7R alpha
146 ation as well as cytolytic activity involves IL-2R beta signals that also up-regulate expression of t
147 , our data support a model in which limiting IL-2R signaling is amplified by thymic Tregs to readily
148 f IL-2-dependent targets is indexed to a low IL-2R signaling threshold and that a substantial proport
149 istinct amounts of IL-2R signaling, with low IL-2R signaling sufficient for many key aspects of Treg
152 n mixed chimeras where the Tregs with mutant IL-2Rs were forced to compete with wild-type Tregs durin
153 ymptoms; IL-2R, IL-12, and transfusion need; IL-2R, IL-8, and leukocytosis; IP-10 and thrombocytopeni
155 ding many of these studies is the ability of IL-2R to deliver redundant mitogenic signals from differ
157 and Treg cells requires distinct amounts of IL-2R signaling, with low IL-2R signaling sufficient for
159 eletion of JH7-6 impaired the association of IL-2R beta and IL-4R alpha chains with Jak1 but did not
160 more, an Ab reactive with the alpha-chain of IL-2R complex reduced the viability mediated by IL-2 sec
162 7R alpha-chain and the cytoplasmic domain of IL-2R beta-chain in IL-2Rbeta(-/-) mice did not prevent
166 on provides explanations for the efficacy of IL-2R antibody therapy in uveitis, and suggests that ant
170 lines stably expressing deletion mutants of IL-2R that fail to activate PI 3-K have questioned the r
175 We questioned whether the restriction of IL-2R gamma-chain (Il-2rgamma)-dependent cytokine signal
176 These findings support the principal role of IL-2R alpha to deliver IL-2 to the signaling complex and
177 perimental efforts to understand the role of IL-2R expression and signaling in the suppressor functio
179 To more precisely define the direct role of IL-2R signaling on CD8(+) T cells during the response to
180 se data suggest that the predominant role of IL-2R signals delivered to responding CD8(+) T cells is
181 regulation, illustrating the specificity of IL-2R beta and gamma subunit signaling on the regulation
183 d characterization of a new genetic stock of IL-2R common gamma-chain deficient NOD/LtSz-scid (NOD-sc
192 ng an adoptive transfer system with IL-2- or IL-2R-deficient TCR transgenic CD8 T cells and MHC class
193 s action is not dependent on either IL-4R or IL-2R signals and results in OX40 controlling initial na
196 y, NK cells do not inhibit IL-2 secretion or IL-2R up-regulation and do not induce T cell death.
199 -205, B7-1, CD4, and interleukin-2 receptor (IL-2R) antibodies and histopathologic, RT-PCR, and delay
201 lasmic domain of the interleukin-2 receptor (IL-2R) beta chain that is involved in the recruitment of
202 expressing the high-affinity IL-2 receptor (IL-2R) consisting of the alpha/p55/CD25, beta/p75/CD122,
209 nes in the interleukin (IL)-2/IL-2 receptor (IL-2R) pathway are associated with type 1 diabetes.
210 ignificantly higher levels of IL-2 receptor (IL-2R) signaling compared with those in lonesome microwe
213 ation, making unclear whether IL-2 receptor (IL-2R) signals ultimately have a predominantly positive
214 nt expression of the interleukin 2 receptor (IL-2R), are reliant on IL-2 produced by activated T cell
215 mma(c) chains of the interleukin-2 receptor (IL-2R), the heavy chain of the major histocompatibility
216 leukin-2 (IL-2) secretion and IL-2 receptor (IL-2R)-signal transducer and activator of transcription
217 donor T cells, their interleukin-2-receptor (IL-2R) alpha-chain expression and their capacity to indu
219 ted that Thr-450 is important for regulating IL-2R complex formation, recruitment of JAK3, and activa
222 ique as monitored by serum levels of soluble IL-2R alpha and/or human beta-2-microglobulin (P <.05, t
223 owth as monitored by serum levels of soluble IL-2R-alpha (sIL-2R-alpha) and soluble beta2-microglobul
229 increased IL-8 and constitutional symptoms; IL-2R, IL-12, and transfusion need; IL-2R, IL-8, and leu
230 domain and the VE-cadherin cytoplasmic tail (IL-2R-VE-cadcyto) was expressed in microvascular endothe
231 under rechallenge conditions that targeting IL-2R by partial mammalian target of rapamycin inhibitio
232 g the activation of CD8(+) T cells, and that IL-2R-dependent activation of the transcription factor S
233 er, these observations strongly suggest that IL-2R signals can activate a pathway leading to NF-kappa
234 ion compared with wild type, suggesting that IL-2R signaling is required for efficient OX40-mediated
242 greatly diminished expression of CD122, the IL-2R/IL-15R beta-chain, and impaired expression of the
246 ceptor tyrosine kinase that signals from the IL-2R, where activating mutations have been found in div
249 L-12 is shown to stimulate expression of the IL-2R alpha-chain (CD25) to much higher levels than are
250 gulated both the p55 and p75 subunits of the IL-2R and enhanced 5- to 10-fold the susceptibility of T
251 ed against the alpha-chain (Tac/CD25) of the IL-2R are an emerging therapy in both transplantation an
255 sisted of the extracytoplasmic domain of the IL-2R beta-chain and the cytoplasmic domain of IL-7R alp
256 how that transgenic thymic expression of the IL-2R beta-chain in IL-2Rbeta-deficient mice prevents le
260 sion of both the p55 and p75 subunits of the IL-2R in T-cell leukemias and p75 in B-cell leukemias.
261 controlling the nonredundant activity of the IL-2R is selective compartmentalization of IL-2-producin
262 te the expression of the three chains of the IL-2R on hDCs and that IL-2 induces STAT5 phosphorylatio
263 ut it was not determined which region of the IL-2R or which pathway was activated to direct this sign
264 helps to explain the interdependence of the IL-2R subunits and Ets1 for NK cell development and func
267 he structure, signaling, and function of the IL-2R, emphasizing the contribution of IL-2 for T cell-d
272 e is required for optimal endocytosis of the IL-2R/ligand complex and is essential for the subsequent
274 G but not anti-CD52 mAb (alemtuzumab) or the IL-2R antagonists causes rapid and sustained expansion o
275 of IL-2Rbeta tyrosines, indicating that the IL-2R engages at least two distinct signaling pathways t
278 owth and differentiation signals through the IL-2R initially favors Ag-specific CD8(+) T cells to dev
280 emain largely unknown, signaling through the IL-2R represents one feature for the production of T(reg
281 t mice and mice unable to signal through the IL-2R, we hypothesized that the tolerizing role of STAT5
282 is inhibited in mice treated with Ab to the IL-2R beta-chain that blocks signaling by either IL-2 or
284 eceptor tyrosine kinases associated with the IL-2R, but in terms of IL-2 signaling, JAK3 but not Lck
285 for treatment of type 1 diabetes within the IL-2R pathway and suggest that an altered IL-2R signalin
289 Our observation may have implications to IL-2R blockade therapy and for the potential role of CD5
290 ation, exhibits a reciprocal relationship to IL-2R expression over the time course of activation of P
294 as proliferation, making it unclear whether IL-2R signals provide a predominantly positive or negati
295 might be due to specificity associated with IL-2R signal transduction or because IL-2 was uniquely p
296 risingly, IL-2R alpha makes no contacts with IL-2R beta or gamma(c), and only minor changes are obser
297 at the immunocytokine associated mainly with IL-2R-expressing innate immune cells, with more bound im
298 The instability primarily occurred with IL-2R(lo) Tregs and was shown, in part, to be the conseq
300 est a rationale for combining rexinoids with IL-2R-targeted therapies in lymphoid malignancies as wel
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