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1 filtrating CD4 helper T cells and CD8 memory cytotoxic T cells.
2 HLA-B27 of presenting antigenic peptides to cytotoxic T cells.
3 fect was associated with a reduced influx of cytotoxic T cells.
4 erized by HA-specific CD4 T helper 1 and CD8 cytotoxic T cells.
5 ing their interaction with SLAMF4-expressing cytotoxic T cells.
6 cells, plasma B cells, and memory helper and cytotoxic T cells.
7 s I loading and cell surface presentation to cytotoxic T cells.
8 modulate immune recognition by NK cells and cytotoxic T cells.
9 euronal death in the presence of appropriate cytotoxic T cells.
10 class I proteins that might be recognized by cytotoxic T cells.
11 xicity and long-term persistence provided by cytotoxic T cells.
12 ules display peptides at the cell surface to cytotoxic T cells.
13 thereby influencing antigen presentation to cytotoxic T cells.
14 vation of antigen-presenting cells and naive cytotoxic T cells.
15 ne production, and their capacities to prime cytotoxic T cells.
16 kidney and used PD-L1 to induce apoptosis of cytotoxic T cells.
17 ecreased infiltration of dendritic cells and cytotoxic T cells.
18 of TNFalpha and YAP1 and low infiltration of cytotoxic T cells.
19 mpaired function of natural killer cells and cytotoxic T cells.
20 tegies, for example those aimed at eliciting cytotoxic T cells.
21 nd to expansion of long-lived tumor-reactive cytotoxic T cells.
22 conclusion, female UCB comprises HY-specific cytotoxic T cells.
23 FN-gamma secreted by CD8+, antigen-specific, cytotoxic T cells.
24 recognition by the T cell receptor (TCR) of cytotoxic T cells.
25 ptides presented on MHC class I molecules to cytotoxic T cells.
26 tly, susceptibility to lysis by PR1-specific cytotoxic T cells.
27 d a decrease in Th1 and granzyme B-producing cytotoxic T cells.
28 e apoptosis of CD4(+) Th1 and Th17 cells and cytotoxic T cells.
29 tary mechanisms, including pathogen-specific cytotoxic T cells.
30 otherapy, and administration of EBV-specific cytotoxic T cells.
31 ne production and generate CD4(+) and CD8(+) cytotoxic T cells.
32 r the induction of relevant epitope-specific cytotoxic T cells.
33 cell surface as potential ligands for CD8(+) cytotoxic T cells.
34 id leukemia cells to generate tumor-specific cytotoxic T cells.
35 reduced expression of cytokines produced by cytotoxic T cells.
36 and targeted for elimination by Ag-specific cytotoxic T cells.
37 reduced signature of markers characterizing cytotoxic T cells.
38 and were infiltrated with mutation-specific cytotoxic T cells.
39 lated membrane attack complex, exotoxins, or cytotoxic T cells.
40 d promote progression through suppression of cytotoxic T cells.
41 rapy promotes the killing of cancer cells by cytotoxic T cells.
44 h defective MHC class I expression, impaired cytotoxic T cell activation, and poor patient prognosis.
45 was normal, in vitro-generated EBV-specific cytotoxic T cell activity was reduced because of CD70 de
48 hese classes of therapeutics is dependent on cytotoxic T-cell activity and is associated with a reduc
49 unction and is a potential target to improve cytotoxic T-cell activity.Grail is an E3 ubiquitin ligas
50 ls and is necessary for efficient priming of cytotoxic T cells against dead cell-associated antigens.
52 nse, interferon-gamma and rejection-induced, cytotoxic T cell and constitutive macrophage-associated
53 pecificity as HLA-A*0201/IMP(58-66)-specific cytotoxic T cells and bound neither to HLA-A*0201 nor th
54 ne response by providing help to B cells and cytotoxic T cells and by releasing different types of cy
55 surface of lymphoma cells for recognition by cytotoxic T cells and can serve as a novel target for de
56 n, but led to increased adhesion of alopecic cytotoxic T cells and enhanced T cell cytotoxicity in an
57 oteins pp65 and IE1 as important inducers of cytotoxic T cells and glycoprotein B (gB) as an importan
58 of mycobacterial-specific polyfunctional and cytotoxic T cells and higher concentrations of Th1 cytok
59 on and promoted elevations in tumor-specific cytotoxic T cells and IFN-gamma levels, while lowering I
60 recruit PA-CXCR4-expressing tumor-targeting cytotoxic T cells and improved the efficacy of adoptive
61 d that AC-NPs induced an expansion of CD8(+) cytotoxic T cells and increased both CD4(+)T/Treg and CD
63 DCs in vivo induced expansion of Ag-specific cytotoxic T cells and inhibited Foxp3(+) regulatory T ce
65 The results showed increased activity of cytotoxic T cells and natural killer cells in BKVN and v
67 nes, and adoptive transfer of tumor-specific cytotoxic T cells and natural killer cells, have been cl
69 cal proteins required for normal function of cytotoxic T cells and NK cells) or secondary (resulting
73 vely kills T helper (Th)1 and Th17 cells and cytotoxic T cells and promotes the immunosuppressive Th2
74 (H)1) response, which leads to activation of cytotoxic T cells and reduction of immunosuppression.
76 tribute to the activation of intraepithelial cytotoxic T cells and the development of villous atrophy
79 ell compartment has more CD4 helper than CD8 cytotoxic T cells, and this is most evident looking at T
80 udies have shown that T helper cells but not cytotoxic T cells are critical for the disease pathology
83 to apoptosis stimuli and the persistence of cytotoxic T cells are essential factors for the outcome
87 e cell types, while CD8(+) T cells (known as cytotoxic T cells) are major cells that provide immunity
88 ls of seven activation markers on helper and cytotoxic T cells as well as the percentage of CD4(+) CD
89 granzyme B, a downstream effector of tumoral cytotoxic T cells, as an early biomarker for tumors resp
93 Immunomodulatory antibodies directed against cytotoxic T cell-associated antigen 4 (CTLA-4/CD152) and
94 g, cytolytic granule composition, type 1 CD8 cytotoxic T cell-associated effector molecules granzyme
95 on susceptibility of melanoma to killing by cytotoxic T cells, blocking SD-4 function enhanced the r
96 signaling provides costimulatory signals to cytotoxic T cells but also increases the frequency of re
97 virus replication initiated by HBV-specific cytotoxic T cells, but it significantly inhibited recrui
99 nd in particular T helper (Th) 1, Th17, CD8+ cytotoxic T cells, CD19+ B cells and CD56+ natural kille
100 endritic cells (CD209(+)), T cells (CD3(+)), cytotoxic T cells (CD8(+)), and helper T cells (CD4(+))
101 11b+), increased dendritic cells (CD86+) and cytotoxic T cells (CD8+) in the p65 knockout (KO) mice.
103 h infiltrating CD4(+) T(H)1 cells and CD8(+) cytotoxic T cells constitute a positive prognostic sign
104 re consistent with a feedback model in which cytotoxic T cells control immune activation by killing d
105 imits vector reapplication, the expansion of cytotoxic T cells correlates with liver inflammation and
107 PCs) within tumors typically do not maintain cytotoxic T cell (CTL) function, despite engaging them.
108 ERK) antigen, the action of antigen-specific cytotoxic T cell (CTL) in vivo results in the emergence
110 hetic subunit vaccines need to induce CD8(+) cytotoxic T cell (CTL) responses for effective vaccinati
111 ontrol of hepatitis C virus (HCV) infection, cytotoxic T cells (CTL) are pivotal, but persistence of
118 donorderived cytomegalovirus (CMV)-specific cytotoxic T cells (CTLs) and compare outcomes with a gro
120 nhanced the frequency of T-helper/memory and cytotoxic T cells (CTLs) in peripheral blood mononuclear
121 se Peripheral blood-derived antigen-specific cytotoxic T cells (CTLs) provide a readily available sou
123 (n = 4), naive (n = 3) and activated (n = 3) cytotoxic T cells (CTLs), and natural killer (NK) (n = 4
124 of tumour antigens that can activate CD8(+) cytotoxic T cells (CTLs), but the microenvironment of es
127 esults suggest that broad, highly functional cytotoxic T cells (cytotoxic T lymphocytes [CTLs]) again
132 lived memory CD8 T cells; however, effective cytotoxic T-cell differentiation occurred only in the pr
136 se of cytokines by T-cell receptor-activated cytotoxic T cells engaged by BiTE antibodies and leading
137 T cell-specific coreceptor CD4 in helper and cytotoxic T cells exemplifies this process, with enhance
139 s are surrounded and invaded by CD8-positive cytotoxic T cells expressing the alphabeta-T cell recept
140 Consequently, alloreactive HLA-A2-specific cytotoxic T cells failed to recognize HLA-A2-expressing
142 tractive method to generate large numbers of cytotoxic T cells for immunotherapy of cancer and viral
143 effective tools to isolate rare high-avidity cytotoxic T cells from patients for use in adoptive ther
147 e cells can similarly modulate the degree of cytotoxic T-cell function and activity in the tumour mic
149 glycosylation of alpha dystroglycan with the cytotoxic T cell glycan and increases the overexpression
150 glycosylation of alpha dystroglycan with the cytotoxic T cell glycan or increased expression of dystr
151 first time that resistance of kidney TEC to cytotoxic T-cell granzyme B-induced death in vitro and i
153 ture types), and killer cells (consisting of cytotoxic T cells, helper T cells, effector B cells, and
155 nalyzed epithelial cells and intraepithelial cytotoxic T cells in family members of patients with cel
159 ammatory infiltrate indicated a reduction of cytotoxic T cells in the post-treatment muscle biopsies
162 ed more potent IFN-gamma-producing and lytic cytotoxic T cells in wt mice compared with NS5A-Tg mice.
163 te an important role for TNF-alpha-producing cytotoxic T-cells in mediating the anti-cancer effects o
164 ectively; (3) increased CD4+ helper and CD8+ cytotoxic T-cells in the spleen; and (4) profound spleni
166 virotherapy with talimogene laherparepvec on cytotoxic T cell infiltration and therapeutic efficacy o
167 led gene expression signatures indicative of cytotoxic T cell infiltration, an interferon-gamma (IFN-
171 Binding and crosslinking of CEACAM-6 by cytotoxic T cells inhibited their activation and resulte
172 l. (2013) reprogram mature, antigen-specific cytotoxic T cells into induced pluripotent stem cells (i
174 illance network of antibodies and sensitized cytotoxic T cells is the extraordinary incidence of lymp
176 in blood cell composition (notably exhausted cytotoxic T cells), it is less clear what explains the o
178 dy, mimicking one of the major mechanisms of cytotoxic T cell killing, inhibits B cell receptor-media
181 IL-2 superkine induced superior expansion of cytotoxic T cells, leading to improved antitumour respon
182 elper T cells TH1 and TH2 serum antibody and cytotoxic T-cell levels compared to bolus controls.
186 rammed death-1 antibody) to ipilimumab (anti-cytotoxic T-cell lymphocyte-associated 4 antibody) in pa
187 including the programmed death 1 (PD-1) and cytotoxic T-cell lymphocyte-associated antigen 4 (CTLA-4
188 8+ lymphocyte infiltration and expression of cytotoxic T-cell markers and effector cytokines, similar
190 ockade that can be mediated by activation of cytotoxic T cells may be overcome in some tumor microenv
191 esented by Li et al shows that memory CD8(+) cytotoxic T cells mediate fibrosis via the secretion of
192 mine the mechanisms by which intraepithelial cytotoxic T cells mediate tissue destruction in celiac d
194 ) cell frequency correlated with inefficient cytotoxic T cell-mediated killing of HTLV-1-infected cel
197 e tumour immune microenvironment and promote cytotoxic-T-cell-mediated tumour regression without targ
199 nce of local immune suppression, transferred cytotoxic T cells more effectively controlled tumors in
200 cells, we were able to stimulate peripheral cytotoxic T cells obtained from colorectal cancer patien
201 Effective immune surveillance by CD8(+) cytotoxic T cells of intracellular microbes and cancer d
203 a is a chronic clonal lymphoproliferation of cytotoxic T cells often associated with autoimmune disea
204 e relevance of Bim in regulating survival of cytotoxic T cells or induction of hepatocyte death has o
206 unosuppressive agents, rituximab, autologous cytotoxic T cells, or cytotoxic chemotherapy often resul
207 Monocyte, natural killer (NK) cell, and cytotoxic T-cell p11 levels were positively associated w
209 immunological control, primarily mediated by cytotoxic T cells, plays a critical role in preventing C
211 associated with infiltrating regulatory and cytotoxic T-cell populations, suggesting distinct immuno
212 delayed SIVsmE660 acquisition; SIV-specific cytotoxic T cells, prechallenge CD4(+) effector memory,
213 aining expression of an efficient type 1 CD8 cytotoxic T cell program (granzyme B(+), IFN-gamma(+)).
214 a and rejection induced (GRIT), quantitative cytotoxic T-cell (QCAT), quantitative constitutive and a
218 ecently demonstrated that differentiation of cytotoxic T cells requires cooperation between T-cell re
222 ENCA mitochondrial lysate vaccine elicited a cytotoxic T cell response in vivo and conferred durable
224 plays an important role in the dysregulated cytotoxic T cell response to HIV-1, and in silico algori
230 oparticle, PC7A NP, which generates a strong cytotoxic T-cell response with low systemic cytokine exp
231 es and high viremia, Cl13 generated a robust cytotoxic T-cell response, resulting in thrombocytopenia
234 t MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth.
237 lated cancers are usually designed to elicit cytotoxic T cell responses by targeting the HPV-16 E7 on
238 rsistent-latent virus that elicits different cytotoxic T cell responses characterized as acute resolv
239 played by these alleles and drive helper and cytotoxic T cell responses in patients with Parkinson's
240 ion of this receptor led to enhanced in vivo cytotoxic T cell responses to apoptotic cell-associated
241 booster vaccination significantly increased cytotoxic T cell responses to subdominant highly conserv
249 pamycin completely abolished vaccine-induced cytotoxic T-cell responses and therapeutic activity.
250 th the ability to stimulate antigen-specific cytotoxic T-cell responses during tumor development.
253 nsfected and endogenous antigens and enhance cytotoxic T-cell responses, indicating that these enzyme
262 lines, together with engineered RMS-directed cytotoxic T cells specific for the fetal acetylcholine r
264 sociated with an increase in T-helper cells, cytotoxic T cells, T-cell functional response, and TCR c
265 ing cells increased over time exclusively on cytotoxic T cells, T-helper cells, and regulatory T cell
266 Here we identified a specialized group of cytotoxic T cells (TC cells) that expressed the chemokin
268 actors T-bet and Eomesodermin (Eomes) in CD8 cytotoxic T cells (Tc), which are key in rejecting tumor
269 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells (TC1), and CD4(+) TH1 cells, which pro
270 hese cells, which we have called 'follicular cytotoxic T cells' (TFC cells), required the transcripti
273 s) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC
274 m this provirus are immunogenic, stimulating cytotoxic T cells that kill RCC cells in vitro and in vi
275 e data reinforce and extend previous data on cytotoxic T cells that one of the principal functions of
276 eventually, the activation of tumor-specific cytotoxic T cells, their recruitment into the tumor site
278 ze ( approximately 50 kDa) that can redirect cytotoxic T cells through simultaneous binding of tumor
280 lls and tumor-associated antigens to recruit cytotoxic T cells to cancer cells, are a promising new a
281 The resulting alphaCLL1-alphaCD3 recruits cytotoxic T cells to CLL1 positive cells, and demonstrat
284 h epithelial stress to allow intraepithelial cytotoxic T cells to kill epithelial cells and induce vi
286 onclassical Qa-1(b)-peptide complexes direct cytotoxic T cells to targets with defective antigen proc
287 represent a novel immunotherapy that bridges cytotoxic T cells to tumor cells, thereby inducing targe
288 ive transfer of donor-derived virus-specific cytotoxic T cells (VSTs) is a strategy to rapidly restor
289 ive transfer of donor-derived viral-specific cytotoxic T-cells (VSTs) is an effective treatment for c
290 d Th17-associated transcription factors, and cytotoxic T cells was found in the gastric lamina propri
291 ination of Nlrc5(Delta/Delta) lymphocytes by cytotoxic T cells was markedly reduced and, in addition,
292 known about resistance mechanisms of RMS to cytotoxic T cells, we investigated RMS cell lines and bi
297 macrophages express cytokines that stimulate cytotoxic T cells, whereas macrophages in neoplastic and
299 BV viral loads and impaired EBV-specific CD8 cytotoxic T cells, with impaired cytokine responses to E
300 umor immunity by directly stimulating CD8(+) cytotoxic T cells, with the potential to increase curati
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