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1 substantial reduction in the number of tumor cytotoxic T lymphocytes.
2 nding and presenting immunogenic peptides to cytotoxic T lymphocytes.
3 or NFATc1 controls the cytotoxicity of mouse cytotoxic T lymphocytes.
4 humans that is normally eliminated by CD8(+) cytotoxic T lymphocytes.
5 important for activation and persistence of cytotoxic T lymphocytes.
6 and increased activation of antigen-specific cytotoxic T lymphocytes.
7 nodes and cross-present antigen to activate cytotoxic T lymphocytes.
8 n of infected or transformed cells by CD8(+) cytotoxic T lymphocytes.
9 man pathogen that is kept in check by CD8(+) cytotoxic T lymphocytes.
10 more H-ras mutations and fewer DMBA-specific cytotoxic T lymphocytes.
11 d engagement with their cognate receptors on cytotoxic T lymphocytes.
12 fected cells, thereby evading elimination by cytotoxic T-lymphocytes.
14 correlated with the presence of CD8-positive cytotoxic T lymphocytes among tumor cells (P < .01) and
15 Here, we engineer human beta-cell-specific cytotoxic T lymphocytes and demonstrate that T1-IFN augm
16 main effector molecules expressed by CD8(+) cytotoxic T lymphocytes and function to destroy allogene
17 vertebrate immune system and is secreted by cytotoxic T lymphocytes and natural killer cells to help
19 tributed to the activation of tumor-reactive cytotoxic T lymphocytes and/or natural killer cells.
21 programmed cell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) immune checkpo
23 checkpoint inhibitors (ICIs), including anti-cytotoxic T lymphocyte antigen 4 (CTLA-4), anti-programm
25 which efforts have focused in particular on cytotoxic T lymphocyte antigen 4 (CTLA4) and PD1, both o
26 inhibitor-based immunotherapies that target cytotoxic T lymphocyte antigen 4 (CTLA4) or the programm
27 ntibodies targeting the checkpoint molecules cytotoxic T lymphocyte antigen 4 (CTLA4), programmed cel
28 death ligand-1 (PD-1/PD-L1), but not through cytotoxic T lymphocyte antigen 4 (CTLA4), was shown to b
29 kers for differentiation (CD127) and anergy (cytotoxic T lymphocyte antigen 4 [CTLA-4] and programmed
30 e been developed include ipilimumab, an anti-cytotoxic T lymphocyte antigen 4 antibody that enhances
31 ell-negative costimulatory molecules such as cytotoxic T lymphocyte antigen-4 (CTLA-4) and programmed
32 ers of regulatory T cells (Tregs), increased cytotoxic T lymphocyte antigen-4 (CTLA-4) expression, an
36 New immune checkpoint inhibitors blocking cytotoxic T lymphocyte antigen-4 (CTLA4) or programmed d
38 provement in response to abatacept, a CTLA4 (cytotoxic T lymphocyte antigen-4)-immunoglobulin fusion
39 nt of immune checkpoint inhibitors targeting cytotoxic T-lymphocyte antigen 4 (CTLA-4) and programmed
40 ssion of programmed death 1 (PD-1) and lower cytotoxic T-lymphocyte antigen 4 (CTLA-4) expression tha
41 on tumor-infiltrating T lymphocytes, such as cytotoxic T-lymphocyte antigen 4 (CTLA-4) molecules are
43 The dNP2-conjugated cytoplasmic domain of cytotoxic T-lymphocyte antigen 4 (dNP2-ctCTLA-4) negativ
44 pression (programmed cell death 1 [PD-1] and cytotoxic T-lymphocyte antigen 4 [CTLA-4]) was similar t
45 defensin, beta 4A [DEFB4A]) or dermal (IL22, cytotoxic T-lymphocyte antigen 4 [CTLA4], and CCR7) and
47 T-cell responses, blocking antibodies (anti-cytotoxic T-lymphocyte antigen 4, anti-programmed death
48 a human monoclonal antibody targeted against cytotoxic T-lymphocyte antigen 4, has shown promise in t
49 of metastatic urothelial carcinoma, tubulin, cytotoxic T-lymphocyte antigen 4, Hsp27, and p53 are nov
50 and overexpression of regulatory molecules (cytotoxic T-lymphocyte antigen 4, programmed cell death
51 e assessed age-specific effects of CTLA4-Ig (cytotoxic T-lymphocyte antigen 4-Ig), a fusion protein b
53 ed in a murine tumor xenograft model of anti-cytotoxic T-lymphocyte antigen-4 (CTLA-4) immunotherapy
54 tors, programmed death receptor-1 (PD-1) and cytotoxic T-lymphocyte antigen-4 (CTLA-4), respectively,
55 bitor), alone or combined with ipilimumab (a cytotoxic T-lymphocyte antigen-4 checkpoint inhibitor),
56 nd 1 expression, BRAF status, and best prior cytotoxic T-lymphocyte antigen-4 therapy response, then
58 uded patients, 17 received therapy targeting cytotoxic T-lymphocyte antigen-4, and 85 received monoth
61 ckpoint therapy that revives tumour-reactive cytotoxic T lymphocytes, are effective in some patients(
63 , such as programmed cell death 1 (PD-1) and cytotoxic T-lymphocyte associated protein 4 (CTLA4), dow
64 ived >60 days in anti-CD154 (MR1)-treated or cytotoxic T-lymphocyte associated protein 4 (CTLA4)-Ig-t
65 of immune checkpoint pathways, in particular cytotoxic T-lymphocyte associated protein 4 and programm
66 grammed death (PD)-1, PD ligand (PD-L)1, and cytotoxic T lymphocyte-associated antigen (CTLA)-4, is e
67 ckpoint blockade with antibodies that target cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and
68 in the expression of the inhibitory molecule cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) on
70 ocking inhibitory immune checkpoints such as cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) or
71 ponsive beige-like anchor protein (LRBA) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) defi
72 nuclear factor kappaB-inducing kinase (NIK), cytotoxic T lymphocyte-associated antigen 4 (CTLA4), B-c
73 med death 1 (PD-1) or its ligand (PD-L1) and cytotoxic T lymphocyte-associated antigen 4, as well as
74 markers, including FOXP3, CD25, Helios, and cytotoxic T lymphocyte-associated antigen 4; and impaire
76 h in vitro blockade of programmed death-1 or cytotoxic T lymphocyte-associated antigen-4 increased T-
77 atory markers FOXP3, programmed death-1, and cytotoxic T lymphocyte-associated antigen-4 was examined
78 y (anti-CTLA4 DVD, where CTLA4 is defined as cytotoxic T lymphocyte-associated antigen-4) possessing
80 las (TCGA) demonstrate reduced expression of cytotoxic T lymphocyte-associated genes and IFN-gamma-in
81 kpoint blockade with antibodies specific for cytotoxic T lymphocyte-associated protein (CTLA)-4 or pr
82 une checkpoint inhibitory antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and
83 ng the induction of the checkpoint molecules cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and
84 D-1), programmed death ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) for
85 1/programmed death ligand 1 (PD-1/PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) res
86 s programmed cell death protein 1 (PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4), wh
87 3 and immunosuppressive molecules, IL-10 and cytotoxic T lymphocyte-associated protein 4 (CTLA-4).
88 1:programmed death ligand 1 (PD-1:PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4):B7-
89 ath protein (PD) 1-PD ligand 1/2 pathway and cytotoxic T lymphocyte-associated protein 4 are currentl
90 ng fractions of programmed cell death 1 high/cytotoxic T lymphocyte-associated protein 4 high (PD-1hi
91 gulatory markers IL-10, forkhead box P3, and cytotoxic T lymphocyte-associated protein 4 in the soil
92 ical trials investigating the combination of cytotoxic T lymphocyte-associated protein 4 inhibitors a
93 anti-programmed cell death protein 1 or anti-cytotoxic T lymphocyte-associated protein 4 is currently
95 have been reported, favored by the fact that cytotoxic T lymphocyte-associated protein pathway has an
96 mmune checkpoint inhibitors (ICIs) targeting cytotoxic T lymphocyte-associated protein-4 (CTLA-4) and
97 ity in vivo, in line with elevated levels of cytotoxic T-lymphocyte-associated 4 (CTLA-4) protein, bu
98 ment with checkpoint inhibitor antibodies to cytotoxic T-lymphocyte-associated antigen 4 (a-CTLA-4) a
99 tance: Checkpoint blockade therapy targeting cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and
100 by negative regulators of T-cell activation, cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and
101 D-1] checkpoint inhibitor) and ipilimumab (a cytotoxic T-lymphocyte-associated antigen 4 [CTLA-4] che
102 geted (BRAF or MEK) or an immune checkpoint (cytotoxic T-lymphocyte-associated antigen 4 [CTLA-4] or
103 tic virus) in combination with ipilimumab (a cytotoxic T-lymphocyte-associated antigen 4 checkpoint i
104 anti-programmed cell death-1 (PD-1) or anti-cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) ant
106 pilimumab, a monoclonal antibody that blocks cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) sig
107 and this tolerance was dependent on CTLA-4 (cytotoxic T-lymphocyte-associated antigen-4) signaling.
108 activity, which resulted in up-regulation of cytotoxic T-lymphocyte-associated Protein 4 (CTLA-4) and
109 stigated the biophysical interaction between cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and
111 py targeting the immune checkpoint receptors cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and
112 oxp1 and Foxp3 coordinated the regulation of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) exp
114 IM-3), lymphocyte activation gene-3 (LAG-3), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), cl
115 cHL is highly enriched for non-T-regulatory, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)-pos
116 treated with monoclonal antibodies blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4; an
117 ein 1 (PD-1) and its ligand PD-L1 as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA4) have
119 r 2 (TLR2), which regulates the induction of cytotoxic T-lymphocyte-associated protein 4 (CTLA4).
121 G1 monoclonal antibody directed against the cytotoxic T-lymphocyte-associated protein 4 receptor tha
122 checkpoint blockade established by targeting cytotoxic T-lymphocyte-associated protein 4 with ipilimu
123 e that dual aOX40 (anti-CD134)/aCTLA-4 (anti-cytotoxic T-lymphocyte-associated protein 4) immunothera
124 stigate whether tremelimumab, an anti-CTLA4 (cytotoxic T-lymphocyte-associated protein 4) inhibitor,
125 alpha, interleukin-2, interleukin-7, CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), T-cell rec
126 had COPD, with a panel of CD45, CD28, CTLA4 (cytotoxic T-lymphocyte-associated protein 4), tumor necr
127 tion of the autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (C
128 potential treatment, with administration of cytotoxic T-lymphocyte-associated protein 4-Ig reducing
130 NE study, we investigated the effects of the cytotoxic-T-lymphocyte-associated antigen 4 (CTLA-4) mon
131 checkpoint blockade using antibodies against cytotoxic-T-lymphocyte-associated protein 4 (CTLA4) or p
132 checkpoint blocking (ICB) antibodies against cytotoxic-T-lymphocyte-associated protein 4 or programme
133 window to impede protective immunity through cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4).
134 ration programs through inhibitory receptor, cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4).
135 ia have shown that the regulatory molecules, cytotoxic T-lymphocyte attenuator-4 (CTLA-4), lymphocyte
136 es of differential escape could aid rational cytotoxic T-lymphocyte-based vaccine immunogen selection
137 omplex (MHC) class I molecule HLA-A2 produce cytotoxic T lymphocytes bearing T cell receptors (TCRs)
138 sing the MHC class I molecule HLA-A2 produce cytotoxic T lymphocytes bearing T-cell receptors (TCRs)
139 the new mouse line is an ideal tool to study cytotoxic T lymphocyte biology and to optimize personali
142 ed to correlate well with the populations of cytotoxic T lymphocytes (CD8(+)) and T helper (CD4(+)) c
144 eradication is accomplishable by recruiting cytotoxic T lymphocytes, concomitant with downregulation
146 CMV replication in the same organs where CD4 cytotoxic T lymphocyte (CTL) activity was observed.
148 The immunological synapse formed between a cytotoxic T lymphocyte (CTL) and an infected or transfor
149 immunodeficiencies characterized by impaired cytotoxic T lymphocyte (CTL) and natural killer (NK) cel
151 e transcription factor T-bet is critical for cytotoxic T lymphocyte (CTL) differentiation, but it is
154 ing in-house bioinformatics pipelines, since cytotoxic T lymphocyte (CTL) escape can occur at differe
155 to downregulate MHC-I molecules and enhance cytotoxic T lymphocyte (CTL) evasion in human immunodefi
156 n causes the deterioration of virus-specific cytotoxic T lymphocyte (CTL) function and survival.
159 t represents an important induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathog
160 ategies that induce establish optimal CD8(+) cytotoxic T lymphocyte (CTL) memory for pathogens like t
162 ls should induce DSA synthesis but not naive cytotoxic T lymphocyte (CTL) precursors' priming via dir
163 es of clonal proliferation or HIV-1-specific cytotoxic T lymphocyte (CTL) pressure shape the provirus
164 id transcriptional changes that occur during cytotoxic T lymphocyte (CTL) proliferation and different
165 high-resolution mass spectrometry to map the cytotoxic T lymphocyte (CTL) proteome and the effect of
166 ortantly, rapamycin treatment did not impair cytotoxic T lymphocyte (CTL) recognition and killing of
168 g tumour-specific adaptive immunity, such as cytotoxic T lymphocyte (CTL) response, can result in pro
174 , DTA-1-induced IL-9 promoted tumor-specific cytotoxic T lymphocyte (CTL) responses by enhancing the
176 ighlighted the ability of HIV to escape from cytotoxic T lymphocyte (CTL) responses that concurrently
178 ates have different MxB sensitivities due to cytotoxic T lymphocyte (CTL) selected differences in Gag
179 gnaling modules into complexes that redirect cytotoxic T lymphocyte (CTL) specificity and function in
180 dust mite (HDM) challenge without affecting cytotoxic T lymphocyte (CTL), Th1 cell, or Th17 cell res
189 of HIV.IMPORTANCE In HIV infection, although cytotoxic T lymphocytes (CTL) play a potentially critica
191 ased gene signature, and the ratio of CD8(+) cytotoxic T lymphocytes (CTL) to CD68(+) macrophages bot
192 understanding of the mechanisms employed by cytotoxic T lymphocytes (CTL) to control tumors will aid
193 eless be efficiently cleared by infiltrating cytotoxic T lymphocytes (CTL) without compromising tumor
197 mount a large, persistently activated CD8(+) cytotoxic T-lymphocyte (CTL) response against HTLV-I-inf
198 To understand the interplay between host cytotoxic T-lymphocyte (CTL) responses and the mechanism
199 thodology for stimulating strong CD8alpha(+) cytotoxic T-lymphocyte (CTL) responses remains lacking.
201 unosuppression (RIS), rituximab (from 2000), cytotoxic T-lymphocyte (CTL) therapy (available in 1999-
202 unosuppression (RIS), rituximab (from 2000), cytotoxic T-lymphocyte (CTL) therapy (available in 1999-
204 ciated with strong and potent HIV-1-specific cytotoxic-T-lymphocyte (CTL) responses restricted by pro
205 Here we show that CD8(+) T-cell (also called cytotoxic T lymphocytes, CTL) feedback activates the NLR
206 eral blood-derived, melanoma-reactive CD8(+) cytotoxic T lymphocytes (CTLs) alone is generally insuff
207 ol: increased infiltration and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenti
208 a persistent infection, while v2.2 generated cytotoxic T lymphocytes (CTLs) and cleared virus within
209 8-2, facilitate cytolytic granule release by cytotoxic T lymphocytes (CTLs) and natural killer (NK) c
210 effects of adaptive and innate immune cells-cytotoxic T lymphocytes (CTLs) and natural killer (NK) c
211 rved in cytolytic lymphocytes-including CD8+ cytotoxic T lymphocytes (CTLs) and natural killer cells-
212 nce of neutrophil NETs interfering cytolytic cytotoxic T lymphocytes (CTLs) and NK cell contacts with
213 Immunological synapse formation between cytotoxic T lymphocytes (CTLs) and the target cells they
217 These therapies are based on the idea that cytotoxic T lymphocytes (CTLs) directly recognize and re
220 apies that boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) have shown promise; howev
221 ls (FDCs), low frequencies of virus-specific cytotoxic T lymphocytes (CTLs) in B cell follicles, expa
222 e of influenza A virus (IAV)-specific CD8(+) cytotoxic T lymphocytes (CTLs) in heterosubtypic cross-p
223 abody) for in vivo molecular imaging of CD8+ cytotoxic T lymphocytes (CTLs) in response to anti-PD-L1
224 tion and numerical reduction of HBV-specific cytotoxic T lymphocytes (CTLs) in the liver and peripher
225 ive cell transfer utilizing tumour-targeting cytotoxic T lymphocytes (CTLs) is one of the most effect
231 tion of tumor antigen-specific (TA-specific) cytotoxic T lymphocytes (CTLs) present within tumors fro
233 es show, however, that DC vaccine priming of cytotoxic T lymphocytes (CTLs) requires the activity of
234 o examine how cytomegalovirus (CMV)-specific cytotoxic T lymphocytes (CTLs) respond to allogeneic ant
236 of these proteins also occurs from activated cytotoxic T lymphocytes (CTLs) where they have recently
238 study the dynamics of virus replication and cytotoxic T lymphocytes (CTLs) within a metapopulation o
239 virus-specific immune mechanisms, including cytotoxic T lymphocytes (CTLs), can clear infected cells
240 of producing clinical-grade BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed with antileukemi
241 including studies on tumor-infiltrating CD8+ cytotoxic T lymphocytes (CTLs), have led to new immunoth
242 le cancer cells to evade killing mediated by cytotoxic T lymphocytes (CTLs), we performed genome-wide
254 broad, highly functional cytotoxic T cells (cytotoxic T lymphocytes [CTLs]) against the HIV-1 Gag pr
256 els of let-7 expression, while generation of cytotoxic T lymphocytes depends upon T cell receptor-med
257 only in tristetraprolin-deficient mice after cytotoxic T lymphocyte depletion, but also in WSX-1/tris
259 utologous, ex vivo expanded, virus-specific, cytotoxic T-lymphocytes derived from HIV-infected patien
260 ptive transfer of donor-derived EBV-specific cytotoxic T-lymphocytes (EBV-CTLs) can eradicate EBV-ass
261 ate that NFATc1 is an important regulator of cytotoxic T lymphocyte effector functions.NFAT nuclear t
262 et al. (2016) showed that forces exerted by cytotoxic T lymphocytes enhance the function of the pore
264 nt reservoir also contains a large number of cytotoxic T lymphocyte escape mutants, presenting anothe
266 regulatory pathway for IL-27 expression and cytotoxic T lymphocyte function mediated by tristetrapro
267 molecular imaging of PD-L1 and CD8 revealed cytotoxic T lymphocytes in the tumor microenvironment in
271 ed the growth of liver metastases, driven by cytotoxic T-lymphocyte-mediated antitumor immunity.
272 attenuates liver carcinogenesis and induces cytotoxic T-lymphocyte-mediated regression of establishe
273 der characterized by unbridled activation of cytotoxic T lymphocytes, natural killer (NK) cells, and
274 mour regression that is dependent on neither cytotoxic T lymphocytes nor humoral immune response.
276 A public alphabetaTCR is identified from the cytotoxic T lymphocytes of patients with carbamazepine-S
278 of elimination of these cells by either the cytotoxic T lymphocyte response or other immune cell sub
279 which has been shown to effectively mount a cytotoxic T lymphocyte response through enhanced tumor i
281 T lymphocytes, suggesting a robust adaptive cytotoxic T-lymphocyte response may, in part, confer res
282 apes the tumour microenvironment and induces cytotoxic T lymphocyte responses against an independent
284 he HLA alleles C*03:03/C*03:04 no allogeneic cytotoxic T-lymphocyte responses are detected in vitro.
285 nnate effector natural killer (NK) cells and cytotoxic T-lymphocyte responses to leukemia-associated
286 human activated autoreactive CD8(+) T-cell (cytotoxic T lymphocyte) responses within the islets of p
288 d T-cell intracytoplasmic antigen 1-positive cytotoxic T lymphocytes, suggesting a robust adaptive cy
289 y ZMYND8 causes breast cancer cells to evade cytotoxic T-lymphocyte surveillance, which leads to tumo
290 ave also been investigated in detail; CD4(+) cytotoxic T lymphocytes (suspected of promoting disease)
291 Upon contact with antigen-presenting cells, cytotoxic T lymphocytes (T cells) establish a highly org
293 entiation of naive CD8 T cells into effector cytotoxic T lymphocytes upon antigen stimulation is nece
295 en and interacted directly with infiltrating cytotoxic T lymphocytes, which led to macrophage depleti
296 ticulum, herpes simplex virus is hidden from cytotoxic T lymphocytes, which may contribute to establi
297 nock-ins, which are viable and fertile, have cytotoxic T lymphocytes with endogeneously fluorescent c
298 frequent peripheral antigen-specific CD8(+) cytotoxic T lymphocytes with immune memory than IFA-emul
299 1 upregulation protects them from killing by cytotoxic T lymphocytes, yet dampens the antitumor respo
300 od to reveal that sorting the most migratory cytotoxic T lymphocytes yields a pool of cells with enha