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1 e clearance of the treated cells mediated by cytotoxic T cells.
2 nd increasing the number of tumor-associated cytotoxic T cells.
3 lectively and its effects on intraepithelial cytotoxic T cells.
4 of TNFalpha and YAP1 and low infiltration of cytotoxic T cells.
5 recognition by the T cell receptor (TCR) of cytotoxic T cells.
6 tly, susceptibility to lysis by PR1-specific cytotoxic T cells.
7 reduced expression of cytokines produced by cytotoxic T cells.
8 and targeted for elimination by Ag-specific cytotoxic T cells.
9 reduced signature of markers characterizing cytotoxic T cells.
10 and were infiltrated with mutation-specific cytotoxic T cells.
11 lated membrane attack complex, exotoxins, or cytotoxic T cells.
12 d promote progression through suppression of cytotoxic T cells.
13 atively activated intestinal intraepithelial cytotoxic T cells.
14 rapy promotes the killing of cancer cells by cytotoxic T cells.
15 filtrating CD4 helper T cells and CD8 memory cytotoxic T cells.
16 HLA-B27 of presenting antigenic peptides to cytotoxic T cells.
17 fect was associated with a reduced influx of cytotoxic T cells.
18 erized by HA-specific CD4 T helper 1 and CD8 cytotoxic T cells.
19 ing their interaction with SLAMF4-expressing cytotoxic T cells.
20 cells, plasma B cells, and memory helper and cytotoxic T cells.
21 s I loading and cell surface presentation to cytotoxic T cells.
22 modulate immune recognition by NK cells and cytotoxic T cells.
23 euronal death in the presence of appropriate cytotoxic T cells.
24 class I proteins that might be recognized by cytotoxic T cells.
25 xicity and long-term persistence provided by cytotoxic T cells.
26 ules display peptides at the cell surface to cytotoxic T cells.
27 al clearance is mediated by the functions of cytotoxic T cells.
28 electively bind peptides for presentation to cytotoxic T cells.
29 dedifferentiated cell state upon exposure to cytotoxic T cells.
30 ctivity of immune cells, including decreased cytotoxic T cells.
31 with blood vessel dysfunction and a lack of cytotoxic T cells.
32 r growth in mice in a manner that depends on cytotoxic T cells.
33 romoting robust intratumoral infiltration of cytotoxic T cells.
34 SOX4 expression and sensitizes TNBC cells to cytotoxic T cells.
35 ty to recognition and elimination by cognate cytotoxic T cells.
36 cally activated inflammatory macrophages and cytotoxic T cells.
37 ol for HLA presentation of HIV-1 epitopes to cytotoxic T cells.
38 exosomes in facilitating the suppression of cytotoxic T cells.
39 rget MHC I molecules to avoid recognition by cytotoxic T cells.
40 ene silencing and promote tumor clearance by cytotoxic T cells.
41 such as immune-stimulatory myeloid cells and cytotoxic T cells.
42 e highest CD68 expression and associate with cytotoxic T-cells.
45 Treatment with tamoxifen increases liver cytotoxic T cell accumulation and reduces colon cancer L
46 ting these pathways can indirectly stimulate cytotoxic T cell activation and recruitment, and synergi
47 h defective MHC class I expression, impaired cytotoxic T cell activation, and poor patient prognosis.
50 was normal, in vitro-generated EBV-specific cytotoxic T cell activity was reduced because of CD70 de
52 hese classes of therapeutics is dependent on cytotoxic T-cell activity and is associated with a reduc
53 generate neo-antigenic epitopes that elicit cytotoxic T-cell activity and subsequent pressure to sel
54 unction and is a potential target to improve cytotoxic T-cell activity.Grail is an E3 ubiquitin ligas
56 nse, interferon-gamma and rejection-induced, cytotoxic T cell and constitutive macrophage-associated
57 pecificity as HLA-A*0201/IMP(58-66)-specific cytotoxic T cells and bound neither to HLA-A*0201 nor th
58 ne response by providing help to B cells and cytotoxic T cells and by releasing different types of cy
59 y collagen were less efficient at attracting cytotoxic T cells and capable of inhibiting T cell proli
60 mesothelioma through systemic activation of cytotoxic T cells and enhanced production of IFN-gamma a
61 ed numbers of bone marrow-infiltrating OX40+ cytotoxic T cells and helper T cells, as well as decreas
62 recruit PA-CXCR4-expressing tumor-targeting cytotoxic T cells and improved the efficacy of adoptive
63 d that AC-NPs induced an expansion of CD8(+) cytotoxic T cells and increased both CD4(+)T/Treg and CD
65 tumors had significantly few CD8(+)/PD-1(+) cytotoxic T cells and more CD25(+)/FOXP3(+) regulatory T
67 The results showed increased activity of cytotoxic T cells and natural killer cells in BKVN and v
69 s, granzyme B production by cytotoxic cells (cytotoxic T cells and natural killer cells), and interle
70 nes, and adoptive transfer of tumor-specific cytotoxic T cells and natural killer cells, have been cl
73 cal proteins required for normal function of cytotoxic T cells and NK cells) or secondary (resulting
76 ll lines to differentiation antigen-specific cytotoxic T cells and observe strong enrichment of a pre
78 by an increase in stromal CD8(+)IFNgamma(+) cytotoxic T cells and significant attenuation of tumor c
80 tribute to the activation of intraepithelial cytotoxic T cells and the development of villous atrophy
88 e cell types, while CD8(+) T cells (known as cytotoxic T cells) are major cells that provide immunity
89 hological features (invasion of myofibres by cytotoxic T cells) are unique among muscle diseases.
90 ls of seven activation markers on helper and cytotoxic T cells as well as the percentage of CD4(+) CD
91 granzyme B, a downstream effector of tumoral cytotoxic T cells, as an early biomarker for tumors resp
93 2-low asthma exhibit an airway deficiency in cytotoxic T cells associated with obesity-driven inflamm
94 Immunomodulatory antibodies directed against cytotoxic T cell-associated antigen 4 (CTLA-4/CD152) and
95 g, cytolytic granule composition, type 1 CD8 cytotoxic T cell-associated effector molecules granzyme
96 umoral infiltration and activation of CD8(+) cytotoxic T cells, attenuated growth of pancreatic neopl
97 ) is inversely associated with the levels of cytotoxic T cell-attracting chemokines (C-C motif chemok
98 signaling provides costimulatory signals to cytotoxic T cells but also increases the frequency of re
100 nd in particular T helper (Th) 1, Th17, CD8+ cytotoxic T cells, CD19+ B cells and CD56+ natural kille
101 11b+), increased dendritic cells (CD86+) and cytotoxic T cells (CD8+) in the p65 knockout (KO) mice.
105 PCs) within tumors typically do not maintain cytotoxic T cell (CTL) function, despite engaging them.
106 ERK) antigen, the action of antigen-specific cytotoxic T cell (CTL) in vivo results in the emergence
107 hetic subunit vaccines need to induce CD8(+) cytotoxic T cell (CTL) responses for effective vaccinati
110 ontrol of hepatitis C virus (HCV) infection, cytotoxic T cells (CTL) are pivotal, but persistence of
114 tory signaling that enhances the activity of cytotoxic T cells (CTLs) could identify potential target
115 nhanced the frequency of T-helper/memory and cytotoxic T cells (CTLs) in peripheral blood mononuclear
116 se Peripheral blood-derived antigen-specific cytotoxic T cells (CTLs) provide a readily available sou
118 (n = 4), naive (n = 3) and activated (n = 3) cytotoxic T cells (CTLs), and natural killer (NK) (n = 4
119 of tumour antigens that can activate CD8(+) cytotoxic T cells (CTLs), but the microenvironment of es
121 First, ovalbumin (OVA) antigen-specific cytotoxic T-cells (CTLs) were incubated with N-azidoacet
122 esults suggest that broad, highly functional cytotoxic T cells (cytotoxic T lymphocytes [CTLs]) again
124 ned treatment limited tumor progression in a cytotoxic T-cell-dependent manner, as depletion of CD8(+
131 nt cohorts revealed strong associations with cytotoxic T-cell dysfunction and exclusion, respectively
134 T cell-specific coreceptor CD4 in helper and cytotoxic T cells exemplifies this process, with enhance
136 tractive method to generate large numbers of cytotoxic T cells for immunotherapy of cancer and viral
137 actions were significantly lower, while CD8+ cytotoxic T cell fractions were significantly higher, co
138 effective tools to isolate rare high-avidity cytotoxic T cells from patients for use in adoptive ther
141 viral interference with the ultimate step in cytotoxic T cell function, the death of infected cells.
143 e cells can similarly modulate the degree of cytotoxic T-cell function and activity in the tumour mic
145 glycosylation of alpha dystroglycan with the cytotoxic T cell glycan and increases the overexpression
146 glycosylation of alpha dystroglycan with the cytotoxic T cell glycan or increased expression of dystr
147 first time that resistance of kidney TEC to cytotoxic T-cell granzyme B-induced death in vitro and i
149 ture types), and killer cells (consisting of cytotoxic T cells, helper T cells, effector B cells, and
152 tudy supports a role for both regulatory and cytotoxic T cells in determining cancer risk among healt
154 nalyzed epithelial cells and intraepithelial cytotoxic T cells in family members of patients with cel
155 D-1 and interleukin-10 (IL-10) expression by cytotoxic T cells in H5N1 (2:6)-infected mice, suggestin
157 nsion of circulating plasmablasts and CD4(+) cytotoxic T cells in patients with IgG(4)-related diseas
159 ty to activate both CD4(+) helper and CD8(+) cytotoxic T cells in response to necrotic cells and may
162 te an important role for TNF-alpha-producing cytotoxic T-cells in mediating the anti-cancer effects o
163 ectively; (3) increased CD4+ helper and CD8+ cytotoxic T-cells in the spleen; and (4) profound spleni
164 s formed in WNT5A knockout mice had elevated cytotoxic T cells, increased M1 macrophages, and decreas
166 virotherapy with talimogene laherparepvec on cytotoxic T cell infiltration and therapeutic efficacy o
167 ress, antiviral pathways, IFN signaling, and cytotoxic T cell infiltration in human cancers, while a
168 led gene expression signatures indicative of cytotoxic T cell infiltration, an interferon-gamma (IFN-
169 in EOC tissue and inversely correlated with cytotoxic T cell infiltration, suggesting that HE4 may c
174 on of Th-1 chemokines, migration of Th-1 and cytotoxic T cells into the tumor, and activation of immu
178 ction in TAMs the percentage of infiltrating cytotoxic T cells is increased, indicating a change in t
180 in blood cell composition (notably exhausted cytotoxic T cells), it is less clear what explains the o
183 dy, mimicking one of the major mechanisms of cytotoxic T cell killing, inhibits B cell receptor-media
184 nergizes with CBI to expand and reinvigorate cytotoxic T cells, leading to superb anticancer efficacy
185 elper T cells TH1 and TH2 serum antibody and cytotoxic T-cell levels compared to bolus controls.
186 d activated T cells, naive helper T (Th) and cytotoxic T cells, loss of CD56bright regulatory NK cell
188 patients in our analysis, 32 resumed an anti-cytotoxic T-cell lymphocyte-4 (CTLA-4) agent, and 135 an
189 rammed death-1 antibody) to ipilimumab (anti-cytotoxic T-cell lymphocyte-associated 4 antibody) in pa
191 8+ lymphocyte infiltration and expression of cytotoxic T-cell markers and effector cytokines, similar
193 ockade that can be mediated by activation of cytotoxic T cells may be overcome in some tumor microenv
194 esented by Li et al shows that memory CD8(+) cytotoxic T cells mediate fibrosis via the secretion of
195 mine the mechanisms by which intraepithelial cytotoxic T cells mediate tissue destruction in celiac d
196 INCR1 knockdown sensitizes tumor cells to cytotoxic T cell-mediated killing, improving CAR T cell
200 e tumour immune microenvironment and promote cytotoxic-T-cell-mediated tumour regression without targ
201 nce of local immune suppression, transferred cytotoxic T cells more effectively controlled tumors in
202 cells, we were able to stimulate peripheral cytotoxic T cells obtained from colorectal cancer patien
203 Effective immune surveillance by CD8(+) cytotoxic T cells of intracellular microbes and cancer d
204 a is a chronic clonal lymphoproliferation of cytotoxic T cells often associated with autoimmune disea
205 Monocyte, natural killer (NK) cell, and cytotoxic T-cell p11 levels were positively associated w
207 immunological control, primarily mediated by cytotoxic T cells, plays a critical role in preventing C
208 howed the highest CLA(+)/CLA(-) T(H)1/type 1 cytotoxic T-cell polarization, with parallel T(H)2/T(H)9
212 associated with infiltrating regulatory and cytotoxic T-cell populations, suggesting distinct immuno
213 a and rejection induced (GRIT), quantitative cytotoxic T-cell (QCAT), quantitative constitutive and a
214 LA-B from the cell surface in order to evade cytotoxic-T-cell recognition, while leaving HLA-C and HL
215 ts and were extensively infiltrated by mouse cytotoxic T cells, reflecting a vigorous host anti-tumor
216 ENCA mitochondrial lysate vaccine elicited a cytotoxic T cell response in vivo and conferred durable
218 rotection against T. parva involves a CD8(+) cytotoxic T cell response to parasite-infected cells.
219 T cell clonal expansions and diminishes the cytotoxic T cell response to subsequent infections, lead
225 oparticle, PC7A NP, which generates a strong cytotoxic T-cell response with low systemic cytokine exp
226 es and high viremia, Cl13 generated a robust cytotoxic T-cell response, resulting in thrombocytopenia
227 potentially be used in vaccines to increase cytotoxic T cell responses against Ags that are targeted
229 t MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth.
230 lated cancers are usually designed to elicit cytotoxic T cell responses by targeting the HPV-16 E7 on
231 rsistent-latent virus that elicits different cytotoxic T cell responses characterized as acute resolv
232 played by these alleles and drive helper and cytotoxic T cell responses in patients with Parkinson's
233 booster vaccination significantly increased cytotoxic T cell responses to subdominant highly conserv
245 conditions of tumour cells induced systemic cytotoxic T-cell responses and immunological memory asso
246 pamycin completely abolished vaccine-induced cytotoxic T-cell responses and therapeutic activity.
247 th the ability to stimulate antigen-specific cytotoxic T-cell responses during tumor development.
248 s II region only, implying the importance of cytotoxic T-cell responses for the former and CD4(+) T-c
249 ized by a macrophage-mediated improvement of cytotoxic T-cell responses through the induction of cyto
252 nsfected and endogenous antigens and enhance cytotoxic T-cell responses, indicating that these enzyme
259 oteolysis promoted early clonal expansion of cytotoxic T cells resulting in an 8-fold increase over T
260 sequencing studies; the presence of a marked cytotoxic T cell signature in gene expression studies; a
261 with high antigen presentation machinery and cytotoxic T cell signature scores are found to have a pr
263 surements included total T cells, helper and cytotoxic T-cell subsets, naive and memory phenotype of
265 sociated with an increase in T-helper cells, cytotoxic T cells, T-cell functional response, and TCR c
266 ing cells increased over time exclusively on cytotoxic T cells, T-helper cells, and regulatory T cell
268 Here we identified a specialized group of cytotoxic T cells (TC cells) that expressed the chemokin
270 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells (TC1), and CD4(+) TH1 cells, which pro
271 hese cells, which we have called 'follicular cytotoxic T cells' (TFC cells), required the transcripti
272 s) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC
273 b responses against the sporozoite stage and cytotoxic T cells that eliminate parasite-infected hepat
274 eventually, the activation of tumor-specific cytotoxic T cells, their recruitment into the tumor site
276 lls and tumor-associated antigens to recruit cytotoxic T cells to cancer cells, are a promising new a
277 The resulting alphaCLL1-alphaCD3 recruits cytotoxic T cells to CLL1 positive cells, and demonstrat
279 a host innate immune system and reactivates cytotoxic T cells to elicit durable response in some can
281 h epithelial stress to allow intraepithelial cytotoxic T cells to kill epithelial cells and induce vi
286 -DQ8 have a crucial role in the licensing of cytotoxic T cells to mediate intestinal epithelial cell
287 reviously unappreciated capability of CD8(+) cytotoxic T cells to penetrate into a large target, T. g
288 represent a novel immunotherapy that bridges cytotoxic T cells to tumor cells, thereby inducing targe
289 at can be effectively challenged by adoptive cytotoxic T cell transfer (ACT)-based immunotherapy.
290 ive transfer of donor-derived virus-specific cytotoxic T cells (VSTs) is a strategy to rapidly restor
291 ive transfer of donor-derived viral-specific cytotoxic T-cells (VSTs) is an effective treatment for c
296 macrophages express cytokines that stimulate cytotoxic T cells, whereas macrophages in neoplastic and
299 izes MDSCs and triggers the rapid accrual of cytotoxic T cells, with consequent tumor clearance poten
300 umor immunity by directly stimulating CD8(+) cytotoxic T cells, with the potential to increase curati