コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 velop nonresponsiveness and exhibit elevated activation-induced cell death.
2 lls, but are insufficient to protect against activation-induced cell death.
3 DN mice despite the resistance of T cells to activation-induced cell death.
4 play distinct roles in T cell activation and activation-induced cell death.
5 ion point and enter S phase, show defects in activation-induced cell death.
6 appeared to be related to the inhibition of activation-induced cell death.
7 older RasGRP1lag mice and were resistant to activation-induced cell death.
8 neously at the expense of low thresholds for activation-induced cell death.
9 s and matrix metalloproteinases, and reduced activation-induced cell death.
10 or-specific T-cell number was due to reduced activation-induced cell death.
11 d CD8-deficient mice, indicating a defect in activation-induced cell death.
12 heral blood T cells and also is critical for activation-induced cell death.
13 ing, leading to cytokine gene expression and activation-induced cell death.
14 cide mechanism involved in the phenomenon of activation-induced cell death.
15 ivation in vitro and in vivo, rapidly die by activation-induced cell death.
16 use Ag-stimulated T cells are susceptible to activation-induced cell death.
17 oliferative response of T cells or promoting activation-induced cell death.
18 ule, Fas ligand (FasL), which contributes to activation-induced cell death.
19 (null) T cells are protected from undergoing activation-induced cell death.
20 and increased susceptibility of Th cells to activation-induced cell death.
21 scriptional activation of cytokine genes and activation-induced cell death.
22 of CD40/CD154-dependent cell activation and activation-induced cell death.
23 ning lymphocyte homeostasis by signaling for activation-induced cell death.
24 must then be eliminated, a process known as activation-induced cell death.
25 her mediates cell growth and protection from activation-induced cell death.
26 phocytes and to rescue effector T cells from activation-induced cell death.
27 oimmune cells, costimulation of T cells, and activation-induced cell death.
28 that is independent from the role of IL-2 in activation-induced cell death.
29 tial to elicit the NFAT-dependent program of activation-induced cell death.
30 oimmune cells, costimulation of T cells, and activation-induced cell death.
31 ion of CD43 protected T cell hybridomas from activation-induced cell death.
32 lls and the mouse T cell hybridoma A1.1 from activation-induced cell death.
33 f T lymphocytes and primes T lymphocytes for activation-induced cell death.
34 interleukin-2-deficient mice did not undergo activation-induced cell death.
35 Fas (CD95) are involved in the regulation of activation-induced cell death.
36 ipheral immune system is achieved in part by activation-induced cell death.
37 al elimination by a form of apoptosis termed activation-induced cell death.
38 as due in part to an increased resistance to activation-induced cell death.
39 tory for B-cell lymphoma growth by signaling activation-induced cell death.
40 anisms including accumulation in tissues and activation-induced cell death.
41 monstrate that the FasR is not necessary for activation-induced cell death.
42 cue CD4 T cells from apoptosis, but enhances activation-induced cell death.
43 ly, but utilize different pathways to signal activation-induced cell death.
44 tween rest and activation and protected from activation-induced cell death.
45 ssion indicates their high susceptibility to activation-induced cell death.
46 ng both proliferative activity and excessive activation-induced cell death.
47 pients, which is likely mediated by specific activation-induced cell death.
48 ultimately results in their subset-specific, activation-induced cell death.
49 phosphorylated AKT protein and were prone to activation-induced cell death.
50 ergic cells with decreased proliferation and activation-induced cell death.
51 rously than CD4(+) Tcon, and is resistant to activation-induced cell death.
52 L expression after restimulation and undergo activation-induced cell death.
53 tissue where IGRP was expressed followed by activation-induced cell death.
54 tivation but did not affect proliferation or activation-induced cell death.
55 ntiation of regulatory T cells, and mediates activation-induced cell death.
56 ells deficient for NF-kappaB activation from activation-induced cell death.
57 absence of Nod1 and Nod2 primed T cells for activation-induced cell death.
58 beta-catenin may mediate protection against activation-induced cell death.
59 ator of this disease, through attenuation of activation-induced cell death.
60 hese mice showed more proliferation and less activation-induced cell death.
61 ion did not reveal a role for TRAIL-mediated activation-induced cell death.
62 rred CD8(+) T cells were lost, likely due to activation-induced cell death.
63 S-dependent JNK activation that leads to its activation-induced cell death.
64 er population, being the most susceptible to activation-induced cell death.
65 ed changes in morphology and protection from activation-induced cell death.
66 lly regulate immune activation, by mediating activation-induced cell death.
67 induces NFATc1/alphaA and proliferation, but activation-induced cell death after 3-d incubation in vi
68 roliferation and increased susceptibility to activation-induced cell death after antigen exposure.
69 of the in vivo response undergo very little activation-induced cell death after sterile FACS sorting
70 te two "new" properties of HO-1 that mediate activation induced cell death (AICD) of allo-antigen-res
71 ed at high TMr-GAD concentrations because of activation-induced cell death (AICD) after initial proli
72 ally, we found that h1218-CART19 had reduced activation-induced cell death (AICD) and enhanced expans
73 The converted DN T cells were resistant to activation-induced cell death (AICD) and expressed a uni
74 nt C57BL/6 (CD22(-/-[B6])) mice that undergo activation-induced cell death (AICD) and fail to up-regu
78 -cell receptor pathway signals the so-called activation-induced cell death (AICD) essential for immun
79 to prime NK and T cells for Fas/TNF-mediated activation-induced cell death (AICD) fits nicely with th
80 es were analyzed for their susceptibility to activation-induced cell death (AICD) in response to CD3/
89 evaluated a strategy to selectively enhance activation-induced cell death (AICD) of anti-recipient T
92 -phase MHC class I/peptide monomers to cause activation-induced cell death (AICD) of previously activ
97 sms for the protective effect of VIP against activation-induced cell death (AICD) of Th2 effectors.
98 ated by functional inactivation (anergy) and activation-induced cell death (AICD) or apoptosis throug
101 ation of TCRs on stimulated T cells leads to activation-induced cell death (AICD) resulting in the do
102 athway involving p53 contributes to the high activation-induced cell death (AICD) susceptibility of r
103 as (lpr) or FasL (gld) are more resistant to activation-induced cell death (AICD) than normal T cells
106 nd (FasL) on activated T lymphocytes induces activation-induced cell death (AICD), and also triggers
107 ng Tregs (suppressor T cells), IL-2-mediated activation-induced cell death (AICD), and the cytokine T
108 25 -/- T cells are resistant to Fas-mediated activation-induced cell death (AICD), and this defect ca
110 ptor (TCR)-mediated apoptosis, also known as activation-induced cell death (AICD), plays an important
111 ribed immunomodulation by glucocorticoids on activation-induced cell death (AICD), the effects of dex
112 y activated T cells to undergo apoptosis, or activation-induced cell death (AICD), upon T-cell recept
113 ole of IRS in the protection of T cells from activation-induced cell death (AICD), we transfected the
114 d that reducing susceptibility of T cells to activation-induced cell death (AICD), which increases du
115 eliminated by an apoptotic process known as activation-induced cell death (AICD), which requires the
129 two separate types of cell death can occur (activation-induced cell death and activated T cell auton
130 tact-mediated and secreted vesicle-generated activation-induced cell death and also demonstrates that
131 y in MAIDS includes a TCR-induced program of activation-induced cell death and an uncoupling from cyt
132 as or its cognate ligand lead to inefficient activation-induced cell death and are specific causes of
133 ne metabolism of the MDSCs themselves led to activation-induced cell death and conversion of MDSCs to
134 , nitric oxide also seems to be required for activation-induced cell death and elimination of T cells
135 phenylalanine) resulted in the inhibition of activation-induced cell death and Fas ligand up-regulati
136 mune shutdown with heightened sensitivity to activation-induced cell death and Fas-independent apopto
137 may be an important molecular determinant of activation-induced cell death and GVHD pathogenesis.
138 c in the early signaling events that lead to activation-induced cell death and IL-2 production after
139 d T lymphocytes from these mice show reduced activation-induced cell death and increased proliferatio
140 This TIL subset also displays increased activation-induced cell death and mediates specific cyto
142 costimulatory blockade has features of both activation-induced cell death and passive cell death.
143 gh the serine/threonine kinase Pak2 to abate activation-induced cell death and promote survival of CA
145 Inclusion of 4-1BB is critical for reducing activation-induced cell death and promoting survival of
146 The mutation has significant effects on activation-induced cell death and TCR internalization, b
147 cting associations between susceptibility to activation-induced cell death and the cell cycle in T ce
148 of these molecules can potentially result in activation-induced cell death and the subsequent loss of
149 ma (RCC) tumors sensitized normal T cells to activation induced cell death, and the responsible produ
150 cells from the liver, presumably reflecting activation-induced cell death, and by the recruitment of
151 implicated in immune regulation, apoptosis, activation-induced cell death, and control of autoimmuni
152 th Fas and its ligand on T cells, leading to activation-induced cell death, and expression of FasL by
153 bit increased lymphoproliferation, decreased activation-induced cell death, and impaired induction of
154 revealed decreased FasL activity, decreased activation-induced cell death, and increased T cell prol
155 ession in K-ras-activated cells inhibits p38 activation-induced cell death, and inhibition of endogen
156 s in nonlymphoid organs, probably because of activation-induced cell death, and may be important in i
157 cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differ
158 ve to apoptosis induced by crosslinking Fas, activation-induced cell death, and to apoptosis induced
159 tly, these cells lack the ability to undergo activation-induced cell death, and to kill Fas-bearing t
160 ogen-induced proliferation, IL-2 production, activation-induced cell death, and up-regulation of bax
162 absence of GFAP staining was consistent with activation-induced cell death as a mechanism of inflamma
163 that IRF-4-deficient mice display defects in activation-induced cell death, as well as superantigen-i
164 Tim-3(-/-) donor T cells underwent increased activation-induced cell death because of increased IFN-g
165 nd CD4 single-positive thymocytes undergoing activation-induced cell death bind and internalize IL-2.
168 f RORgamma t protects T cell hybridomas from activation-induced cell death by inhibiting the upregula
170 ously activated T cells have been described: activation-induced cell death can be triggered by restim
171 expression, and increases susceptibility to activation-induced cell death, cellular traits that are
172 wer proliferation rate and were resistant to activation-induced cell death compared with DQ8.CD28(+/+
174 ection), TCR down-regulation, and peripheral activation-induced cell death dominated the phenotype of
175 have been shown by others to interfere with activation-induced cell death (e.g. , interleukin-2 [IL-
176 T cells to become sensitive to Fas-mediated activation-induced cell death (Fas-AICD), we examined wh
177 he well-characterized delay in CD95-mediated activation-induced cell death following initial ligation
178 ead are rendered susceptible to Fas-mediated activation-induced cell death following stimulation thro
179 owever, unlike IL-2 treatment, which induces activation-induced cell death, IL-21 sustained CD8(+) T
180 y has previously been demonstrated to induce activation-induced cell death in aggressive histology hu
183 nsgenic mice reversed both susceptibility to activation-induced cell death in CREB-dn T cells and the
184 sis that induction of MINOR would lead to an activation-induced cell death in DCs and that its inhibi
185 and FK506, have been demonstrated to inhibit activation-induced cell death in immature T cells and T
187 nd simplify a novel network corresponding to activation-induced cell death in large granular lymphocy
190 cell proliferation and abrogated S1-specific activation-induced cell death in peripheral blood mononu
191 -cells during thymic development, along with activation-induced cell death in peripheral lymphocytes,
192 o prevent the overstimulation of T cells and activation-induced cell death in settings of chronic ant
194 a signal transduction pathway that leads to activation-induced cell death in T-lymphocytes and invol
195 t also lead to a reduced survival by driving activation-induced cell death in targeted NK cells.
196 herefore, we investigated the role of Shc in activation-induced cell death in these cells by creating
202 astic B-cell growth is believed to occur via activation-induced cell death in which stimuli that typi
204 40 signaling, T reg cells underwent enhanced activation-induced cell death, indicating that OX40 deli
207 loss of mature CD4(+) T cells suggested that activation-induced cell death is a mechanism for helper
208 of intracellular Ca(2+), we have shown that activation-induced cell death is directly proportional t
210 icient C57BL/6-lpr/lpr mice, suggesting that activation-induced cell death limited autoimmunity in no
212 he absence of proliferation, indicating that activation-induced cell death may cause some of the repo
213 ich inhibit T cell proliferation and promote activation induced cell death, may be required to dimini
214 CD4(+) T-cell depletion via a Fas-dependent activation-induced cell death mechanism, along with impa
215 f autoreactive cells relies on Fas-dependent activation-induced cell death mechanisms, an important c
216 TCR-transgenic mice, suggesting that neither activation-induced cell death nor differentiation into T
217 peptide within a short period of time causes activation-induced cell death of Ad5 E1A-specific CTLs.
218 actions have been strongly implicated in the activation-induced cell death of both lymphocytes and ot
219 ate that SHP1 or SHP2 is required to prevent activation-induced cell death of CD4(+) T cells and is c
220 pressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells af
221 onclude that in addition to the promotion of activation-induced cell death of lymphocytes and the gen
222 of target cells by NK cells and CTLs and in activation-induced cell death of mature T lymphocytes.
224 supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cell
226 xx acquires a dispersed nuclear pattern, and activation-induced cell death of splenocytes is profound
227 hese transcriptional defects lead to reduced activation-induced cell death of stimulated Itk-/- T cel
228 evealing the significant contribution to the activation-induced cell death of T cells by downstream c
229 ncreased spontaneous apoptosis and decreased activation-induced cell death of T cells in systemic lup
232 andin endoperoxide E(2) selectively inhibits activation-induced cell death of Th2 cells by signaling
234 enhanced expansion because of GzmB-mediated activation-induced cell death of wild-type CD4(+)CD25(-)
235 part by leukotoxin-mediated apoptosis (i.e., activation-induced cell death) of bovine leukocytes.
236 ific for the virus are sensitized to undergo activation-induced cell death on TCR stimulation in vitr
239 eral tissues where restimulation can lead to activation-induced cell death or do not receive sufficie
240 show that anti-CD137 mAbs can induce T cell activation-induced cell death or enhance antiviral immun
241 Thus, deletion of activated T cells through activation-induced cell death or growth factor withdrawa
242 FasL- or tumor necrosis factor (TNF)-induced activation-induced cell death or on deficiencies of anti
243 id not observe either enhanced resistance to activation-induced cell death or preferential generation
244 cells did not have any alterations in either activation-induced cell death or Th1/2 polarization.
246 not associated with capillary leak syndrome, activation-induced cell death, or with a major effect on
248 of SLE lymphocytes in vitro is caused by an activation-induced cell death process initiated in vivo.
249 heightened susceptibility of CD4 T cells to activation-induced cell death, progressive defects in ce
250 being eliminated by direct virus killing and activation-induced cell death, requires the continuous d
251 appear to use distinct mechanisms, AINR and activation-induced cell death, respectively, to limit ex
253 ype Th1 cells, indicating that resistance to activation-induced cell death significantly enhances T c
254 T3-deficient lymphocytes more susceptible to activation-induced cell death, suggesting that STAT3 mig
255 omoting proliferation, protecting cells from activation-induced cell death, supporting IFN-gamma prod
258 ted splenocytes underwent significantly less activation-induced cell death than B6wt CD4(+) T cells,
259 ing, resulted in antagonism of Fas-dependent activation-induced cell death that was always accompanie
260 ly increases their probability of undergoing activation-induced cell death, thereby inhibiting effect
261 nd maintenance of T regulatory cells and for activation-induced cell death, thereby mediating toleran
262 L-27 has a crucial role in the inhibition of activation-induced cell death, thereby permitting Ag-dri
263 eviously that VIP/PACAP protect T cells from activation-induced cell death through down-regulation of
264 s regulatory role by preventing Fas-mediated activation-induced cell death through inhibition of casp
265 onstrated that this may be due to diminished activation-induced cell death through ITK inhibition.
266 proportion of expanded clones which survives activation-induced cell death to become long term memory
267 he altered NK cell homeostasis resulted from activation-induced cell death triggered by anti-4-1BB.
268 T cells, they were not sufficient to inhibit activation-induced cell death triggered by CD3 cross-lin
269 ant additional cell death signals regulating activation-induced cell death under physiological condit
270 val of CD28(-) CTLs, which were sensitive to activation-induced cell death upon anti-CD3 stimulation.
271 T cells lacking SHP1 and SHP2 show increased activation-induced cell death upon anti-CD3/CD28 stimula
272 te that Fra1, a Fos member of AP-1, enhances activation-induced cell death upon induction in activate
273 TIM1 in T cells was associated with impaired activation-induced cell death upon repeated TCR engageme
274 ndergo rapid Fas/Fas ligand (FasL)-mediated, activation-induced cell death upon restimulation with an
275 nd find that helpless cells undergo death by activation-induced cell death upon secondary stimulation
278 ignificantly impaired, expression of Fas and activation-induced cell death was unaffected in T cells
279 2 signaling but does not inhibit priming for activation-induced cell death, we found that mice with d
281 tic cell death and the anti-CD3 mAb-mediated activation-induced cell death were significantly enhance
282 lls from CD44 KO mice were more resistant to activation-induced cell death when compared with the CD4
283 ells hypoproliferated and exhibited enhanced activation-induced cell death when stimulated with anti-
284 itro, Fas-deficient T cells are resistant to activation-induced cell death, whereas Bcl-2-overexpress
285 s, undergo morphological changes, and resist activation-induced cell death, whereas conventional T ce
286 A central pathway for T-cell apoptosis is activation-induced cell death, which is triggered throug
287 autocrine proliferation but are sensitive to activation-induced cell death, which may cause them to b
288 ber of regulatory T cells and show increased activation-induced cell death, which might contribute to
289 re low, and T cell blasts displayed enhanced activation-induced cell death, which was corrected by ad
290 of T cells by accelerating cell turnover and activation-induced cell death while decreasing the renew