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1 absence of Nod1 and Nod2 primed T cells for activation-induced cell death.
2 DN mice despite the resistance of T cells to activation-induced cell death.
3 play distinct roles in T cell activation and activation-induced cell death.
4 ion point and enter S phase, show defects in activation-induced cell death.
5 appeared to be related to the inhibition of activation-induced cell death.
6 older RasGRP1lag mice and were resistant to activation-induced cell death.
7 neously at the expense of low thresholds for activation-induced cell death.
8 s and matrix metalloproteinases, and reduced activation-induced cell death.
9 or-specific T-cell number was due to reduced activation-induced cell death.
10 d CD8-deficient mice, indicating a defect in activation-induced cell death.
11 heral blood T cells and also is critical for activation-induced cell death.
12 that is independent from the role of IL-2 in 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 as due in part to an increased resistance to activation-induced cell death.
23 of CD40/CD154-dependent cell activation and activation-induced cell death.
24 ning lymphocyte homeostasis by signaling for activation-induced cell death.
25 must then be eliminated, a process known as activation-induced cell death.
26 her mediates cell growth and protection from activation-induced cell death.
27 phocytes and to rescue effector T cells from activation-induced cell death.
28 S-dependent JNK activation that leads to its activation-induced cell death.
29 oimmune cells, costimulation of T cells, and activation-induced cell death.
30 tial to elicit the NFAT-dependent program of activation-induced cell death.
31 anisms including accumulation in tissues and activation-induced cell death.
32 oimmune cells, costimulation of T cells, and activation-induced cell death.
33 ion of CD43 protected T cell hybridomas from activation-induced cell death.
34 lls and the mouse T cell hybridoma A1.1 from activation-induced cell death.
35 f T lymphocytes and primes T lymphocytes for activation-induced cell death.
36 interleukin-2-deficient mice did not undergo activation-induced cell death.
37 Fas (CD95) are involved in the regulation of activation-induced cell death.
38 ipheral immune system is achieved in part by activation-induced cell death.
39 al elimination by a form of apoptosis termed activation-induced cell death.
40 tory for B-cell lymphoma growth by signaling 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 phosphorylated AKT protein and were prone to activation-induced cell death.
45 ergic cells with decreased proliferation and activation-induced cell death.
46 rously than CD4(+) Tcon, and is resistant to activation-induced cell death.
47 L expression after restimulation and undergo activation-induced cell death.
48 tissue where IGRP was expressed followed by activation-induced cell death.
49 ntiation of regulatory T cells, and mediates activation-induced cell death.
50 ells deficient for NF-kappaB activation from activation-induced cell death.
51 beta-catenin may mediate protection against activation-induced cell death.
52 ator of this disease, through attenuation of activation-induced cell death.
53 hese mice showed more proliferation and less activation-induced cell death.
54 ion did not reveal a role for TRAIL-mediated activation-induced cell death.
55 rred CD8(+) T cells were lost, likely due to activation-induced cell death.
56 er population, being the most susceptible to activation-induced cell death.
57 ed changes in morphology and protection from activation-induced cell death.
58 lly regulate immune activation, by mediating activation-induced cell death.
59 velop nonresponsiveness and exhibit elevated activation-induced cell death.
60 lls, but are insufficient to protect against activation-induced cell death.
61 induces NFATc1/alphaA and proliferation, but activation-induced cell death after 3-d incubation in vi
62 of the in vivo response undergo very little activation-induced cell death after sterile FACS sorting
63 te two "new" properties of HO-1 that mediate activation induced cell death (AICD) of allo-antigen-res
64 ed at high TMr-GAD concentrations because of activation-induced cell death (AICD) after initial proli
65 The converted DN T cells were resistant to activation-induced cell death (AICD) and expressed a uni
66 nt C57BL/6 (CD22(-/-[B6])) mice that undergo activation-induced cell death (AICD) and fail to up-regu
70 -cell receptor pathway signals the so-called activation-induced cell death (AICD) essential for immun
71 to prime NK and T cells for Fas/TNF-mediated activation-induced cell death (AICD) fits nicely with th
72 es were analyzed for their susceptibility to activation-induced cell death (AICD) in response to CD3/
81 evaluated a strategy to selectively enhance activation-induced cell death (AICD) of anti-recipient T
84 -phase MHC class I/peptide monomers to cause activation-induced cell death (AICD) of previously activ
89 sms for the protective effect of VIP against activation-induced cell death (AICD) of Th2 effectors.
90 ated by functional inactivation (anergy) and activation-induced cell death (AICD) or apoptosis throug
93 ation of TCRs on stimulated T cells leads to activation-induced cell death (AICD) resulting in the do
94 athway involving p53 contributes to the high activation-induced cell death (AICD) susceptibility of r
95 as (lpr) or FasL (gld) are more resistant to activation-induced cell death (AICD) than normal T cells
98 nd (FasL) on activated T lymphocytes induces activation-induced cell death (AICD), and also triggers
99 ng Tregs (suppressor T cells), IL-2-mediated activation-induced cell death (AICD), and the cytokine T
100 25 -/- T cells are resistant to Fas-mediated activation-induced cell death (AICD), and this defect ca
102 ptor (TCR)-mediated apoptosis, also known as activation-induced cell death (AICD), plays an important
103 ribed immunomodulation by glucocorticoids on activation-induced cell death (AICD), the effects of dex
104 y activated T cells to undergo apoptosis, or activation-induced cell death (AICD), upon T-cell recept
105 ole of IRS in the protection of T cells from activation-induced cell death (AICD), we transfected the
106 d that reducing susceptibility of T cells to activation-induced cell death (AICD), which increases du
107 eliminated by an apoptotic process known as activation-induced cell death (AICD), which requires the
119 two separate types of cell death can occur (activation-induced cell death and activated T cell auton
120 tact-mediated and secreted vesicle-generated activation-induced cell death and also demonstrates that
121 y in MAIDS includes a TCR-induced program of activation-induced cell death and an uncoupling from cyt
122 as or its cognate ligand lead to inefficient activation-induced cell death and are specific causes of
123 , nitric oxide also seems to be required for activation-induced cell death and elimination of T cells
124 phenylalanine) resulted in the inhibition of activation-induced cell death and Fas ligand up-regulati
125 mune shutdown with heightened sensitivity to activation-induced cell death and Fas-independent apopto
126 may be an important molecular determinant of activation-induced cell death and GVHD pathogenesis.
127 c in the early signaling events that lead to activation-induced cell death and IL-2 production after
128 d T lymphocytes from these mice show reduced activation-induced cell death and increased proliferatio
129 This TIL subset also displays increased activation-induced cell death and mediates specific cyto
131 costimulatory blockade has features of both activation-induced cell death and passive cell death.
133 The mutation has significant effects on activation-induced cell death and TCR internalization, b
134 cting associations between susceptibility to activation-induced cell death and the cell cycle in T ce
135 of these molecules can potentially result in activation-induced cell death and the subsequent loss of
136 ma (RCC) tumors sensitized normal T cells to activation induced cell death, and the responsible produ
137 cells from the liver, presumably reflecting activation-induced cell death, and by the recruitment of
138 implicated in immune regulation, apoptosis, activation-induced cell death, and control of autoimmuni
139 th Fas and its ligand on T cells, leading to activation-induced cell death, and expression of FasL by
140 bit increased lymphoproliferation, decreased activation-induced cell death, and impaired induction of
141 revealed decreased FasL activity, decreased activation-induced cell death, and increased T cell prol
142 ession in K-ras-activated cells inhibits p38 activation-induced cell death, and inhibition of endogen
143 s in nonlymphoid organs, probably because of activation-induced cell death, and may be important in i
144 cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differ
145 ve to apoptosis induced by crosslinking Fas, activation-induced cell death, and to apoptosis induced
146 tly, these cells lack the ability to undergo activation-induced cell death, and to kill Fas-bearing t
147 ogen-induced proliferation, IL-2 production, activation-induced cell death, and up-regulation of bax
149 that IRF-4-deficient mice display defects in activation-induced cell death, as well as superantigen-i
150 Tim-3(-/-) donor T cells underwent increased activation-induced cell death because of increased IFN-g
151 nd CD4 single-positive thymocytes undergoing activation-induced cell death bind and internalize IL-2.
154 f RORgamma t protects T cell hybridomas from activation-induced cell death by inhibiting the upregula
156 ously activated T cells have been described: activation-induced cell death can be triggered by restim
157 expression, and increases susceptibility to activation-induced cell death, cellular traits that are
158 wer proliferation rate and were resistant to activation-induced cell death compared with DQ8.CD28(+/+
160 ection), TCR down-regulation, and peripheral activation-induced cell death dominated the phenotype of
161 have been shown by others to interfere with activation-induced cell death (e.g. , interleukin-2 [IL-
162 T cells to become sensitive to Fas-mediated activation-induced cell death (Fas-AICD), we examined wh
163 he well-characterized delay in CD95-mediated activation-induced cell death following initial ligation
164 ead are rendered susceptible to Fas-mediated activation-induced cell death following stimulation thro
165 owever, unlike IL-2 treatment, which induces activation-induced cell death, IL-21 sustained CD8(+) T
166 y has previously been demonstrated to induce activation-induced cell death in aggressive histology hu
169 nsgenic mice reversed both susceptibility to activation-induced cell death in CREB-dn T cells and the
170 sis that induction of MINOR would lead to an activation-induced cell death in DCs and that its inhibi
171 and FK506, have been demonstrated to inhibit activation-induced cell death in immature T cells and T
173 nd simplify a novel network corresponding to activation-induced cell death in large granular lymphocy
176 -cells during thymic development, along with activation-induced cell death in peripheral lymphocytes,
178 a signal transduction pathway that leads to activation-induced cell death in T-lymphocytes and invol
179 herefore, we investigated the role of Shc in activation-induced cell death in these cells by creating
185 astic B-cell growth is believed to occur via activation-induced cell death in which stimuli that typi
187 40 signaling, T reg cells underwent enhanced activation-induced cell death, indicating that OX40 deli
190 loss of mature CD4(+) T cells suggested that activation-induced cell death is a mechanism for helper
191 of intracellular Ca(2+), we have shown that activation-induced cell death is directly proportional t
193 icient C57BL/6-lpr/lpr mice, suggesting that activation-induced cell death limited autoimmunity in no
195 he absence of proliferation, indicating that activation-induced cell death may cause some of the repo
196 ich inhibit T cell proliferation and promote activation induced cell death, may be required to dimini
197 CD4(+) T-cell depletion via a Fas-dependent activation-induced cell death mechanism, along with impa
198 f autoreactive cells relies on Fas-dependent activation-induced cell death mechanisms, an important c
199 TCR-transgenic mice, suggesting that neither activation-induced cell death nor differentiation into T
200 peptide within a short period of time causes activation-induced cell death of Ad5 E1A-specific CTLs.
201 actions have been strongly implicated in the activation-induced cell death of both lymphocytes and ot
202 pressed IFN-gamma production, expansion, and activation-induced cell death of HCV-specific T cells af
203 onclude that in addition to the promotion of activation-induced cell death of lymphocytes and the gen
204 of target cells by NK cells and CTLs and in activation-induced cell death of mature T lymphocytes.
206 supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cell
208 xx acquires a dispersed nuclear pattern, and activation-induced cell death of splenocytes is profound
209 hese transcriptional defects lead to reduced activation-induced cell death of stimulated Itk-/- T cel
210 evealing the significant contribution to the activation-induced cell death of T cells by downstream c
211 ncreased spontaneous apoptosis and decreased activation-induced cell death of T cells in systemic lup
214 andin endoperoxide E(2) selectively inhibits activation-induced cell death of Th2 cells by signaling
216 enhanced expansion because of GzmB-mediated activation-induced cell death of wild-type CD4(+)CD25(-)
217 part by leukotoxin-mediated apoptosis (i.e., activation-induced cell death) of bovine leukocytes.
218 ific for the virus are sensitized to undergo activation-induced cell death on TCR stimulation in vitr
221 eral tissues where restimulation can lead to activation-induced cell death or do not receive sufficie
222 show that anti-CD137 mAbs can induce T cell activation-induced cell death or enhance antiviral immun
223 Thus, deletion of activated T cells through activation-induced cell death or growth factor withdrawa
224 FasL- or tumor necrosis factor (TNF)-induced activation-induced cell death or on deficiencies of anti
225 id not observe either enhanced resistance to activation-induced cell death or preferential generation
226 cells did not have any alterations in either activation-induced cell death or Th1/2 polarization.
228 not associated with capillary leak syndrome, activation-induced cell death, or with a major effect on
230 of SLE lymphocytes in vitro is caused by an activation-induced cell death process initiated in vivo.
231 heightened susceptibility of CD4 T cells to activation-induced cell death, progressive defects in ce
232 being eliminated by direct virus killing and activation-induced cell death, requires the continuous d
233 appear to use distinct mechanisms, AINR and activation-induced cell death, respectively, to limit ex
235 ype Th1 cells, indicating that resistance to activation-induced cell death significantly enhances T c
236 T3-deficient lymphocytes more susceptible to activation-induced cell death, suggesting that STAT3 mig
237 omoting proliferation, protecting cells from activation-induced cell death, supporting IFN-gamma prod
240 ted splenocytes underwent significantly less activation-induced cell death than B6wt CD4(+) T cells,
241 ing, resulted in antagonism of Fas-dependent activation-induced cell death that was always accompanie
242 ly increases their probability of undergoing activation-induced cell death, thereby inhibiting effect
243 nd maintenance of T regulatory cells and for activation-induced cell death, thereby mediating toleran
244 L-27 has a crucial role in the inhibition of activation-induced cell death, thereby permitting Ag-dri
245 eviously that VIP/PACAP protect T cells from activation-induced cell death through down-regulation of
246 s regulatory role by preventing Fas-mediated activation-induced cell death through inhibition of casp
247 onstrated that this may be due to diminished activation-induced cell death through ITK inhibition.
248 proportion of expanded clones which survives activation-induced cell death to become long term memory
249 he altered NK cell homeostasis resulted from activation-induced cell death triggered by anti-4-1BB.
250 T cells, they were not sufficient to inhibit activation-induced cell death triggered by CD3 cross-lin
251 ant additional cell death signals regulating activation-induced cell death under physiological condit
252 val of CD28(-) CTLs, which were sensitive to activation-induced cell death upon anti-CD3 stimulation.
253 te that Fra1, a Fos member of AP-1, enhances activation-induced cell death upon induction in activate
254 TIM1 in T cells was associated with impaired activation-induced cell death upon repeated TCR engageme
255 ndergo rapid Fas/Fas ligand (FasL)-mediated, activation-induced cell death upon restimulation with an
256 nd find that helpless cells undergo death by activation-induced cell death upon secondary stimulation
259 ignificantly impaired, expression of Fas and activation-induced cell death was unaffected in T cells
260 2 signaling but does not inhibit priming for activation-induced cell death, we found that mice with d
262 tic cell death and the anti-CD3 mAb-mediated activation-induced cell death were significantly enhance
263 lls from CD44 KO mice were more resistant to activation-induced cell death when compared with the CD4
264 ells hypoproliferated and exhibited enhanced activation-induced cell death when stimulated with anti-
265 itro, Fas-deficient T cells are resistant to activation-induced cell death, whereas Bcl-2-overexpress
266 s, undergo morphological changes, and resist activation-induced cell death, whereas conventional T ce
267 A central pathway for T-cell apoptosis is activation-induced cell death, which is triggered throug
268 autocrine proliferation but are sensitive to activation-induced cell death, which may cause them to b
269 ber of regulatory T cells and show increased activation-induced cell death, which might contribute to
270 re low, and T cell blasts displayed enhanced activation-induced cell death, which was corrected by ad
271 of T cells by accelerating cell turnover and activation-induced cell death while decreasing the renew
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