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1 nodes and cross-present antigen to activate cytotoxic T lymphocytes.
2 n of infected or transformed cells by CD8(+) cytotoxic T lymphocytes.
3 man pathogen that is kept in check by CD8(+) cytotoxic T lymphocytes.
4 more H-ras mutations and fewer DMBA-specific cytotoxic T lymphocytes.
5 or NFATc1 controls the cytotoxicity of mouse cytotoxic T lymphocytes.
6 substantial reduction in the number of tumor cytotoxic T lymphocytes.
7 d and antitumor immunity was mediated by CD8 cytotoxic T lymphocytes.
8 iminate minimal disease burden by generating cytotoxic T lymphocytes.
9 , and donor or more recently third-party EBV cytotoxic T lymphocytes.
10 of CD73, and thus increasing the activity of cytotoxic T lymphocytes.
11 n of distinct MHC class II-restricted CD4(+) cytotoxic T lymphocytes.
12 nding and presenting immunogenic peptides to cytotoxic T lymphocytes.
13 humans that is normally eliminated by CD8(+) cytotoxic T lymphocytes.
14 fected cells, thereby evading elimination by cytotoxic T-lymphocytes.
16 he antigenic peptide repertoire presented to cytotoxic T lymphocytes and as a result can regulate cyt
17 Here, we engineer human beta-cell-specific cytotoxic T lymphocytes and demonstrate that T1-IFN augm
18 ) presents intracellular-derived peptides to cytotoxic T lymphocytes and its subcellular itinerary is
22 tributed to the activation of tumor-reactive cytotoxic T lymphocytes and/or natural killer cells.
23 xperimental data of the dynamics and role of cytotoxic T lymphocytes, antibodies, and interferon and
24 f ipilimumab, a monoclonal antibody blocking cytotoxic T lymphocyte antigen (CTLA)-4, demonstrates th
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
33 ers of regulatory T cells (Tregs), increased cytotoxic T lymphocyte antigen-4 (CTLA-4) expression, an
39 New immune checkpoint inhibitors blocking cytotoxic T lymphocyte antigen-4 (CTLA4) or programmed d
40 provement in response to abatacept, a CTLA4 (cytotoxic T lymphocyte antigen-4)-immunoglobulin fusion
41 bitory signals in secondary lymphoid organs, cytotoxic T-lymphocyte antigen (CTLA)-4 antibodies media
42 nt of immune checkpoint inhibitors targeting cytotoxic T-lymphocyte antigen 4 (CTLA-4) and programmed
43 ssion of programmed death 1 (PD-1) and lower cytotoxic T-lymphocyte antigen 4 (CTLA-4) expression tha
45 The dNP2-conjugated cytoplasmic domain of cytotoxic T-lymphocyte antigen 4 (dNP2-ctCTLA-4) negativ
46 pression (programmed cell death 1 [PD-1] and cytotoxic T-lymphocyte antigen 4 [CTLA-4]) was similar t
47 defensin, beta 4A [DEFB4A]) or dermal (IL22, cytotoxic T-lymphocyte antigen 4 [CTLA4], and CCR7) and
49 a fully human monoclonal antibody that binds cytotoxic T-lymphocyte antigen 4 to enhance antitumour i
50 checkpoints (eg, programmed cell death 1 and cytotoxic T-lymphocyte antigen 4), are under investigati
51 T-cell responses, blocking antibodies (anti-cytotoxic T-lymphocyte antigen 4, anti-programmed death
52 a human monoclonal antibody targeted against cytotoxic T-lymphocyte antigen 4, has shown promise in t
53 of metastatic urothelial carcinoma, tubulin, cytotoxic T-lymphocyte antigen 4, Hsp27, and p53 are nov
54 and overexpression of regulatory molecules (cytotoxic T-lymphocyte antigen 4, programmed cell death
55 s combined with suboptimal concentrations of cytotoxic T-lymphocyte antigen 4-Ig or cyclosporine.
58 ed in a murine tumor xenograft model of anti-cytotoxic T-lymphocyte antigen-4 (CTLA-4) immunotherapy
59 ssion of the negative costimulatory molecule cytotoxic T-lymphocyte antigen-4 (CTLA-4) on T cells mod
60 via monoclonal antibodies, such as the anti-cytotoxic T-lymphocyte antigen-4 antibody (ipilimumab),
61 bitor), alone or combined with ipilimumab (a cytotoxic T-lymphocyte antigen-4 checkpoint inhibitor),
62 nd 1 expression, BRAF status, and best prior cytotoxic T-lymphocyte antigen-4 therapy response, then
66 ndividuals, immunosuppression is mediated by cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and
67 , such as programmed cell death 1 (PD-1) and cytotoxic T-lymphocyte associated protein 4 (CTLA4), dow
68 of immune checkpoint pathways, in particular cytotoxic T-lymphocyte associated protein 4 and programm
69 ckpoint blockade with antibodies that target cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and
70 in the expression of the inhibitory molecule cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) on
71 ocking inhibitory immune checkpoints such as cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) or
72 atment with monoclonal antibody specific for cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), an
73 A to an aptamer (apt) that selectively binds cytotoxic T lymphocyte-associated antigen 4 (CTLA4(apt))
74 ponsive beige-like anchor protein (LRBA) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) defi
75 nuclear factor kappaB-inducing kinase (NIK), cytotoxic T lymphocyte-associated antigen 4 (CTLA4), B-c
76 w costimulatory blockade agents, such as the cytotoxic T lymphocyte-associated antigen 4-Ig molecule
77 markers, including FOXP3, CD25, Helios, and cytotoxic T lymphocyte-associated antigen 4; and impaire
80 h in vitro blockade of programmed death-1 or cytotoxic T lymphocyte-associated antigen-4 increased T-
81 atory markers FOXP3, programmed death-1, and cytotoxic T lymphocyte-associated antigen-4 was examined
84 las (TCGA) demonstrate reduced expression of cytotoxic T lymphocyte-associated genes and IFN-gamma-in
85 kpoint blockade with antibodies specific for cytotoxic T lymphocyte-associated protein (CTLA)-4 or pr
86 une checkpoint inhibitory antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and
87 1/programmed death ligand 1 (PD-1/PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) res
88 3 and immunosuppressive molecules, IL-10 and cytotoxic T lymphocyte-associated protein 4 (CTLA-4).
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 ical trials investigating the combination of cytotoxic T lymphocyte-associated protein 4 inhibitors a
92 anti-programmed cell death protein 1 or anti-cytotoxic T lymphocyte-associated protein 4 is currently
94 have been reported, favored by the fact that cytotoxic T lymphocyte-associated protein pathway has an
95 tance: Checkpoint blockade therapy targeting cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and
97 D-1] checkpoint inhibitor) and ipilimumab (a cytotoxic T-lymphocyte-associated antigen 4 [CTLA-4] che
98 geted (BRAF or MEK) or an immune checkpoint (cytotoxic T-lymphocyte-associated antigen 4 [CTLA-4] or
99 th melanoma, ipilimumab (an antibody against cytotoxic T-lymphocyte-associated antigen 4 [CTLA-4]) pr
100 tic virus) in combination with ipilimumab (a cytotoxic T-lymphocyte-associated antigen 4 checkpoint i
102 anti-programmed cell death-1 (PD-1) or anti-cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) ant
104 pilimumab, a monoclonal antibody that blocks cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) sig
105 s that promote the function of T cells: anti-cytotoxic T-lymphocyte-associated protein 4 (alpha-CTLA-
106 activity, which resulted in up-regulation of cytotoxic T-lymphocyte-associated Protein 4 (CTLA-4) and
107 ed/refractory acute lymphocytic leukemia and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and
109 IM-3), lymphocyte activation gene-3 (LAG-3), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), cl
110 treated with monoclonal antibodies blocking cytotoxic T-lymphocyte-associated protein 4 (CTLA-4; an
112 r 2 (TLR2), which regulates the induction of cytotoxic T-lymphocyte-associated protein 4 (CTLA4).
114 G1 monoclonal antibody directed against the cytotoxic T-lymphocyte-associated protein 4 receptor tha
115 checkpoint blockade established by targeting cytotoxic T-lymphocyte-associated protein 4 with ipilimu
116 e that dual aOX40 (anti-CD134)/aCTLA-4 (anti-cytotoxic T-lymphocyte-associated protein 4) immunothera
117 alpha, interleukin-2, interleukin-7, CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), T-cell rec
118 tion of the autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (C
119 potential treatment, with administration of cytotoxic T-lymphocyte-associated protein 4-Ig reducing
121 NE study, we investigated the effects of the cytotoxic-T-lymphocyte-associated antigen 4 (CTLA-4) mon
122 checkpoint blockade using antibodies against cytotoxic-T-lymphocyte-associated protein 4 (CTLA4) or p
123 checkpoint blocking (ICB) antibodies against cytotoxic-T-lymphocyte-associated protein 4 or programme
124 ration programs through inhibitory receptor, cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4).
125 window to impede protective immunity through cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4).
126 ia have shown that the regulatory molecules, cytotoxic T-lymphocyte attenuator-4 (CTLA-4), lymphocyte
127 omplex (MHC) class I molecule HLA-A2 produce cytotoxic T lymphocytes bearing T cell receptors (TCRs)
128 sing the MHC class I molecule HLA-A2 produce cytotoxic T lymphocytes bearing T-cell receptors (TCRs)
131 eradication is accomplishable by recruiting cytotoxic T lymphocytes, concomitant with downregulation
132 CMV replication in the same organs where CD4 cytotoxic T lymphocyte (CTL) activity was observed.
134 The immunological synapse formed between a cytotoxic T lymphocyte (CTL) and an infected or transfor
135 immunodeficiencies characterized by impaired cytotoxic T lymphocyte (CTL) and natural killer (NK) cel
139 e transcription factor T-bet is critical for cytotoxic T lymphocyte (CTL) differentiation, but it is
142 ing in-house bioinformatics pipelines, since cytotoxic T lymphocyte (CTL) escape can occur at differe
143 to downregulate MHC-I molecules and enhance cytotoxic T lymphocyte (CTL) evasion in human immunodefi
144 ates to evade host recognition and that CD8+ cytotoxic T lymphocyte (CTL) failure is due to the inabi
145 n causes the deterioration of virus-specific cytotoxic T lymphocyte (CTL) function and survival.
149 t represents an important induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathog
150 ls should induce DSA synthesis but not naive cytotoxic T lymphocyte (CTL) precursors' priming via dir
151 id transcriptional changes that occur during cytotoxic T lymphocyte (CTL) proliferation and different
152 high-resolution mass spectrometry to map the cytotoxic T lymphocyte (CTL) proteome and the effect of
153 ortantly, rapamycin treatment did not impair cytotoxic T lymphocyte (CTL) recognition and killing of
154 assess how the naive epitope-specific CD8(+) cytotoxic T lymphocyte (CTL) repertoire translates to th
157 s are observed in the impact of the dominant cytotoxic T lymphocyte (CTL) response restricted by HLA-
158 als have indicated that AAV capsids induce a cytotoxic T lymphocyte (CTL) response that eliminates tr
159 g tumour-specific adaptive immunity, such as cytotoxic T lymphocyte (CTL) response, can result in pro
162 (iMC), which suppress specific and unrelated cytotoxic T lymphocyte (CTL) responses and are termed my
164 , DTA-1-induced IL-9 promoted tumor-specific cytotoxic T lymphocyte (CTL) responses by enhancing the
166 ous studies have demonstrated that effective cytotoxic T lymphocyte (CTL) responses drive the selecti
167 ighlighted the ability of HIV to escape from cytotoxic T lymphocyte (CTL) responses that concurrently
169 mmunity by adoptive transfer of EBV-specific cytotoxic T lymphocyte (CTL) therapy while highly effect
170 dust mite (HDM) challenge without affecting cytotoxic T lymphocyte (CTL), Th1 cell, or Th17 cell res
171 Anti-human immunodeficiency virus (HIV) cytotoxic T lymphocyte (CTL)-associated epitopes, evolut
172 malarial subunit vaccine inducing protective cytotoxic T lymphocyte (CTL)-mediated immunity could pav
174 ther syntaxin 11 (Stx11) or Munc18-2 abolish cytotoxic T lymphocytes (CTL) and natural killer cell (N
177 donor-derived cytomegalovirus (CMV) specific cytotoxic T lymphocytes (CTL) as immune reconstitution p
180 xamined molecules associated with anergy and cytotoxic T lymphocytes (CTL) in peripheral blood mononu
181 ptively transferred ovalbumin (OVA)-specific cytotoxic T lymphocytes (CTL) induce lung injury in mice
182 of HIV.IMPORTANCE In HIV infection, although cytotoxic T lymphocytes (CTL) play a potentially critica
183 eless be efficiently cleared by infiltrating cytotoxic T lymphocytes (CTL) without compromising tumor
184 ukocytes in tumors, including tumor-specific cytotoxic T lymphocytes (CTL), is altered and results in
185 nvironment, IL-10 inhibits the activation of cytotoxic T lymphocytes (CTL), while IL-12 enhances CTL
192 mount a large, persistently activated CD8(+) cytotoxic T-lymphocyte (CTL) response against HTLV-I-inf
194 To understand the interplay between host cytotoxic T-lymphocyte (CTL) responses and the mechanism
195 thodology for stimulating strong CD8alpha(+) cytotoxic T-lymphocyte (CTL) responses remains lacking.
200 ciated with strong and potent HIV-1-specific cytotoxic-T-lymphocyte (CTL) responses restricted by pro
201 Here we show that CD8(+) T-cell (also called cytotoxic T lymphocytes, CTL) feedback activates the NLR
202 eral blood-derived, melanoma-reactive CD8(+) cytotoxic T lymphocytes (CTLs) alone is generally insuff
204 effects of adaptive and innate immune cells-cytotoxic T lymphocytes (CTLs) and natural killer (NK) c
206 8-2, facilitate cytolytic granule release by cytotoxic T lymphocytes (CTLs) and natural killer (NK) c
208 alysis of CD69 and CD25 levels revealed that cytotoxic T lymphocytes (CTLs) are partially activated i
213 These therapies are based on the idea that cytotoxic T lymphocytes (CTLs) directly recognize and re
216 he tumors that express them, we expanded LMP-cytotoxic T lymphocytes (CTLs) from patients with lympho
218 apies that boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) have shown promise; howev
219 ls (FDCs), low frequencies of virus-specific cytotoxic T lymphocytes (CTLs) in B cell follicles, expa
220 e of influenza A virus (IAV)-specific CD8(+) cytotoxic T lymphocytes (CTLs) in heterosubtypic cross-p
221 tion and numerical reduction of HBV-specific cytotoxic T lymphocytes (CTLs) in the liver and peripher
223 resently assumed that lethal hit delivery by cytotoxic T lymphocytes (CTLs) is mechanistically linked
224 ive cell transfer utilizing tumour-targeting cytotoxic T lymphocytes (CTLs) is one of the most effect
230 tion of tumor antigen-specific (TA-specific) cytotoxic T lymphocytes (CTLs) present within tumors fro
231 o examine how cytomegalovirus (CMV)-specific cytotoxic T lymphocytes (CTLs) respond to allogeneic ant
234 study the dynamics of virus replication and cytotoxic T lymphocytes (CTLs) within a metapopulation o
235 virus-specific immune mechanisms, including cytotoxic T lymphocytes (CTLs), can clear infected cells
237 of producing clinical-grade BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed with antileukemi
238 including studies on tumor-infiltrating CD8+ cytotoxic T lymphocytes (CTLs), have led to new immunoth
239 on of AKT and mTOR are impaired in antiviral cytotoxic T lymphocytes (CTLs), resulting in enhanced ac
250 broad, highly functional cytotoxic T cells (cytotoxic T lymphocytes [CTLs]) against the HIV-1 Gag pr
251 els of let-7 expression, while generation of cytotoxic T lymphocytes depends upon T cell receptor-med
252 only in tristetraprolin-deficient mice after cytotoxic T lymphocyte depletion, but also in WSX-1/tris
254 utologous, ex vivo expanded, virus-specific, cytotoxic T-lymphocytes derived from HIV-infected patien
255 ate that NFATc1 is an important regulator of cytotoxic T lymphocyte effector functions.NFAT nuclear t
256 et al. (2016) showed that forces exerted by cytotoxic T lymphocytes enhance the function of the pore
257 ent soluble and cell-associated tumor Ags to cytotoxic T lymphocytes equally well as BDCA3(+) mDCs.
258 nt reservoir also contains a large number of cytotoxic T lymphocyte escape mutants, presenting anothe
260 regulatory pathway for IL-27 expression and cytotoxic T lymphocyte function mediated by tristetrapro
261 ease in nonmodified CD4(+) T cells, enhanced cytotoxic T lymphocyte function, and antibody responses.
266 ction of regulatory T cells able to suppress cytotoxic T lymphocyte induction in MLCs, and for the ab
268 ization' was reported at the contact area of cytotoxic T lymphocytes interacting with target cells.
269 ed the growth of liver metastases, driven by cytotoxic T-lymphocyte-mediated antitumor immunity.
270 attenuates liver carcinogenesis and induces cytotoxic T-lymphocyte-mediated regression of establishe
271 der characterized by unbridled activation of cytotoxic T lymphocytes, natural killer (NK) cells, and
272 mour regression that is dependent on neither cytotoxic T lymphocytes nor humoral immune response.
275 n the intrinsic characteristics of the naive cytotoxic T lymphocyte precursor pool and extrinsic (lik
276 as vaccines in these mice were deficient in cytotoxic T lymphocytes priming and IL-12 induction in c
278 udovirion (PsV)-based assays, and a vigorous cytotoxic T lymphocyte response by enzyme-linked immunos
280 of elimination of these cells by either the cytotoxic T lymphocyte response or other immune cell sub
281 outgrowing EBV-infected B cells and the EBV cytotoxic T lymphocyte response, and targeting infected
282 ndritic cell is critical for the size of the cytotoxic T lymphocyte response, because dendritic cells
283 T lymphocytes, suggesting a robust adaptive cytotoxic T-lymphocyte response may, in part, confer res
284 apes the tumour microenvironment and induces cytotoxic T lymphocyte responses against an independent
285 was correlated with increased likelihood of cytotoxic T lymphocyte responses and frequency of viral
286 he HLA alleles C*03:03/C*03:04 no allogeneic cytotoxic T-lymphocyte responses are detected in vitro.
287 nnate effector natural killer (NK) cells and cytotoxic T-lymphocyte responses to leukemia-associated
288 human activated autoreactive CD8(+) T-cell (cytotoxic T lymphocyte) responses within the islets of p
291 d T-cell intracytoplasmic antigen 1-positive cytotoxic T lymphocytes, suggesting a robust adaptive cy
293 ed potent bispecific antibodies that recruit cytotoxic T lymphocytes to Her2 and CD20 positive cancer
294 entiation of naive CD8 T cells into effector cytotoxic T lymphocytes upon antigen stimulation is nece
296 stantially reduce the risk of destruction by cytotoxic T lymphocytes, whereas use of alternative sero
297 ticulum, herpes simplex virus is hidden from cytotoxic T lymphocytes, which may contribute to establi
298 surfaces is a key step in the activation of cytotoxic T lymphocytes, which mediate the killing of pa
299 frequent peripheral antigen-specific CD8(+) cytotoxic T lymphocytes with immune memory than IFA-emul
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