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1 important regulator of T cell metabolism and antitumor immunity.
2 ram, which had crippling effects on adaptive antitumor immunity.
3 tumor, where they were modulated to promote antitumor immunity.
4 munotherapeutic payloads leading to systemic antitumor immunity.
5 ion by gammadelta and Th17 cells potentiates antitumor immunity.
6 f IL-10 contribute to CD8(+) T cell-mediated antitumor immunity.
7 tory tumor microenvironment and improve host antitumor immunity.
8 for effective APC-driven local and systemic antitumor immunity.
9 h immunotherapy, promoting radiation-induced antitumor immunity.
10 retion by CD11b(+) DCs prevails and supports antitumor immunity.
11 ICB regulate overlapping pathways to promote antitumor immunity.
12 mmunogenic MC38 tumor cells allows effective antitumor immunity.
13 pansion reduces memory potential and impairs antitumor immunity.
14 n the presence of spontaneous or therapeutic antitumor immunity.
15 comes, credited to their ability to suppress antitumor immunity.
16 onstrated evidence of durable tumor-specific antitumor immunity.
17 dies can lead to tumor clearance and durable antitumor immunity.
18 nment is known to inhibit effective adaptive antitumor immunity.
19 D47-SIRPalpha axis is critical for DC-driven antitumor immunity.
20 rug in its ability to productively stimulate antitumor immunity.
21 eased from the MN patch further augments the antitumor immunity.
22 of miR-155 in T cells, in which it promotes antitumor immunity.
23 mor PD-L1 is not just a marker of suppressed antitumor immunity.
24 ance could lead to new strategies to enhance antitumor immunity.
25 icit poorly understood effects on protective antitumor immunity.
26 overcoming TGF-beta1-induced suppression of antitumor immunity.
27 article formulation of doxorubicin, enhances antitumor immunity.
28 he former of which are superior in mediating antitumor immunity.
29 induce long-lasting CD8(+) T cell-dependent antitumor immunity.
30 s, driven by cytotoxic T-lymphocyte-mediated antitumor immunity.
31 f Th1-mediated and cytotoxic T-cell-mediated antitumor immunity.
32 equently amplify immune response to systemic antitumor immunity.
33 ll cycle activity in cancer cells suppresses antitumor immunity.
34 or reversing immunosuppression and enhancing antitumor immunity.
35 ergy and tumor defense, where it can promote antitumor immunity.
36 sociated sialosides may therefore potentiate antitumor immunity.
37 into T effector cells and leads to enhanced antitumor immunity.
38 mulation in the tumor, resulting in enhanced antitumor immunity.
39 thways responsible for the downregulation of antitumor immunity.
40 ll activation and promotion of CD8(+) T cell antitumor immunity.
41 neoantigen intratumor heterogeneity (ITH) on antitumor immunity.
42 ng, and ultimately depended on CD8(+) T cell antitumor immunity.
43 a serious candidate for the reactivation of antitumor immunity.
44 ated in the nMOF channels to induce systemic antitumor immunity.
45 kdown of human EZH2 in T cells elicited poor antitumor immunity.
46 ), the inhibition of which results in potent antitumor immunity.
47 crucial for in situ MDA-5-induced protective antitumor immunity.
48 onment that might blunt the effectiveness of antitumor immunity.
49 vessel paradigm and discuss its relevance to antitumor immunity.
50 as a candidate therapeutic target to enhance antitumor immunity.
51 cule that limits autoimmunity, antiviral and antitumor immunity.
52 ts tumor-derived DNA and generates intrinsic antitumor immunity.
53 ells (cDCs) is important in host defense and antitumor immunity.
54 hence, they play a role in antimicrobial and antitumor immunity.
55 ctivate a patient's immune system to unleash antitumor immunity.
56 rapeutic costimulatory signaling and restore antitumor immunity.
57 he antigenic breadth and clonal diversity of antitumor immunity.
58 ying cancer cells that can incite protective antitumor immunity.
59 +) cells inhibits tumor growth by augmenting antitumor immunity.
60 by peptide vaccines and enhanced therapeutic antitumor immunity.
61 targeted for enhancing vaccine efficacy and antitumor immunity.
62 upts PD-1-mediated signaling and may restore antitumor immunity.
63 other strategies of Treg ablation to promote antitumor immunity.
64 hereas IFN-gamma production is essential for antitumor immunity.
65 immune responses and may have a key role in antitumor immunity.
66 velopment of metastasis and further enhanced antitumor immunity.
67 be exploited to generate a more efficacious antitumor immunity.
68 ng and selective subset expansion to restore antitumor immunity.
69 associated DC function to support or enhance antitumor immunity.
70 ng effective vaccine induction of protective antitumor immunity.
71 development of multivalent DLL1 to stimulate antitumor immunity.
72 ecific T(mem) that are essential for durable antitumor immunity.
73 role in regulating tumor immunogenicity and antitumor immunity.
74 th 1 is an immune checkpoint that suppresses antitumor immunity.
75 not required for vitiligo or its associated antitumor immunity.
76 n a manner associated with enhanced systemic antitumor immunity.
77 une activation can induce local and systemic antitumor immunity.
78 the immunological synapse in T cell-mediated antitumor immunity.
79 dence of a pDC subset in the TME that favors antitumor immunity.
80 nce for its beneficial role in antiviral and antitumor immunity.
81 hocytes that play key roles in antiviral and antitumor immunity.
82 iated with activation of potent and specific antitumor immunity.
83 and minimal residual disease for generating antitumor immunity.
84 1 and AdipoR2, which are sufficient to blunt antitumor immunity.
85 essive Tregs or MDSCs, resulting in enhanced antitumor immunity.
86 n, as inhibition of STAT3 signaling enhances antitumor immunity.
87 , thus preventing the development of durable antitumor immunity.
88 ed lipid metabolism is essential to maintain antitumor immunity.
89 ines offer a promising approach for inducing antitumor immunity.
90 acquire a dysfunctional state, which limits antitumor immunity.
91 mplicated in potential reinvigoration of the antitumor immunity.
92 in 1 (PD-1; PDCD1), was performed to improve antitumor immunity.
93 gen expression, which could be used to study antitumor immunity.
94 repurposing copper chelators as enhancers of antitumor immunity.
95 nous immune effectors, resulting in improved antitumor immunity.
96 terfere with the proper function of adaptive antitumor immunity.
97 al pH activation, leading to T cell-mediated antitumor immunity.
98 rtance of peptide loading in vaccine-induced antitumor immunity.
99 C1-mediated actions on T cell metabolism and antitumor immunity.
100 activity of Tregs, including suppression of antitumor immunity.
101 mmed cell death protein 1 (PD-1) to suppress antitumor immunity.
102 Chop or ER stress to unleash T cell-mediated antitumor immunity.
103 on of IL-15 in the TME and its importance in antitumor immunity.
104 g pathways to dampen the T-cell response and antitumor immunity.
105 -23 (Ad.scIL-23) was able to induce systemic antitumor immunity.
106 g against AML, which is further augmented by antitumor immunity.
107 lator of interferon genes (STING) pathway in antitumor immunity.
108 mature DCs during imatinib treatment improve antitumor immunity.
109 ent in cancer is thought to primarily affect antitumor immunity.
110 liferation and blockade of this axis rescued antitumor immunity.
111 inhibition is considered a means to enhance antitumor immunity.
112 ectrum of human cancers, where it suppresses antitumor immunity.
113 uppression is crucial for inducing sustained antitumor immunity.
114 rtain contexts, have an inhibitory effect on antitumor immunity, a finding with implications for immu
117 eveal an essential role of LGP2 in promoting antitumor immunity after radiotherapy and provide a new
118 f Ad.E6E7.p16 with Ad.alphaPD1 could improve antitumor immunity against HPV-related tumors and that p
119 tin (TSLP) at a distant site leads to robust antitumor immunity against spontaneous breast carcinogen
120 a tumor-specific antibody fails to generate antitumor immunity against syngeneic B16F10 tumors in mi
121 ancer cells into the circulation, suppresses antitumor immunity allowing circulating cells to survive
122 on of host-microbe interactions that curtail antitumor immunity also present opportunities for interv
123 h helical bodipy show efficient PDT-mediated antitumor immunity amplification with an ultra-low dose
124 sive tumors to secrete galectin-1, dampening antitumor immunity and accelerating malignant progressio
125 uture cases may help elucidate mechanisms of antitumor immunity and allograft tolerance, and inform u
126 immunotherapies are urgently needed to boost antitumor immunity and control disease in cancer patient
127 ated with upregulation of pathways mediating antitumor immunity and corresponding with higher imputed
128 vasculature in the initiation of CD8 T-cell antitumor immunity and demonstrate that tumor endothelia
129 ey mechanism by which tumor PD-L1 suppresses antitumor immunity and demonstrate that tumor PD-L1 is n
130 eviews the mechanisms by which PD-L1 impairs antitumor immunity and discusses established and experim
131 ification of key HNSCC oncogenes that impair antitumor immunity and emerging immune-priming approache
132 established for chronic viral infection and antitumor immunity and has been found to be associated w
135 show that blockade of Fas signaling enhances antitumor immunity and increases survival in a mouse mod
136 -ligand 1 (PD-L1) immune checkpoint augments antitumor immunity and induces durable responses in pati
137 loid-derived suppressor cells (MDSC) subvert antitumor immunity and limit the efficacy of chimeric an
138 hat, in mice, gut commensal microbes promote antitumor immunity and may determine therapy efficacy.
139 f immune evasion co-opted by tumors to evade antitumor immunity and offers an attractive target for c
141 al cells and TAMs to synergistically inhibit antitumor immunity and promote primary colorectal cancer
143 f IL-10 to potentiate CD8(+) T cell-mediated antitumor immunity and provide a potential strategy to i
146 une checkpoint blockade effectively restores antitumor immunity and results in a significant survival
147 une checkpoint blockade effectively restores antitumor immunity and results in a significant survival
148 entify new therapeutic approaches to enhance antitumor immunity and safeguard against autoimmunity.
149 d blockade reduced tumor growth by enhancing antitumor immunity and seemingly reducing angiogenesis i
150 nistic CD40 antibody was sufficient to evoke antitumor immunity and suppress tumor growth in tumor-be
151 administration of 3M-052 generated systemic antitumor immunity and suppressed both injected and dist
152 the cGAS pathway is important for intrinsic antitumor immunity and that cGAMP may be used directly f
153 s of PD-1, which suggests potential roles in antitumor immunity and the response to immunotherapy.
155 trating leukocytes (TILeus) induces systemic antitumor immunity and tumor regression, but not in TME
156 nisms of exosome-mediated resistance against antitumor immunity and we discuss how this resistance co
157 at block PD-1 or PD-L1 facilitate endogenous antitumor immunity and, because of their broad activity
158 ses, immune responses against infection, and antitumor immunity, and accumulating evidence suggests a
159 opment of allospecific transplant tolerance, antitumor immunity, and cross-generational reproductive
160 nted MDSC mobilization, reactivated specific antitumor immunity, and enhanced the antitumor activity
161 osomes accelerates tumor growth by dampening antitumor immunity, and macrophage depletion eliminates
162 t, generates systemic CD8(+) T cell-mediated antitumor immunity, and sensitizes resistant tumors to c
163 umors, induced tumor regression with durable antitumor immunity, and synergized with anti-PD-1 therap
166 use PD-L2 binds to both PD-1, which inhibits antitumor immunity, and to RGMb, which regulates respira
168 ng that the qualitative traits of a specific antitumor immunity are largely dictated by the immunolog
170 noclonal antibody (mAb) drugs that stimulate antitumor immunity are transforming cancer treatment but
171 ng the role of peripheral, clonally directed antitumor immunity as a key mediator of response to PD-1
172 enocarcinoma cells is sufficient to suppress antitumor immunity, as deletion of PD-L1 on highly immun
173 e investigations of early stages of adaptive antitumor immunity, as well as support the rationale for
174 r, systemic inhibition of xCT may compromise antitumor immunity, as xCT is implicated in supporting a
175 7 homolog 1 or CD274) is a major obstacle to antitumor immunity because it tolerizes/anergizes tumor-
176 tential of provoking inflammation to enhance antitumor immunity but also uncover novel host regulatio
177 ive regulatory T cells (Treg cells) suppress antitumor immunity, but how Treg cells behave in the met
178 ate that DNA damage in cancer cells triggers antitumor immunity, but its intrinsic regulatory mechani
179 receptor (CAR) T cells are potent drivers of antitumor immunity, but promoting durable CAR T cell res
180 suppression within the tumor, and reactivate antitumor immunity, but they have yet to live up to thei
182 okines induces a potent antitumor effect and antitumor immunity by ameliorating the immunosuppressive
186 play an active role in suppressing melanoma antitumor immunity by modulating miR-92, which increases
188 emonstrate that GITR co-stimulation mediates antitumor immunity by promoting TH9 cell differentiation
189 and inhibit immune cell activity can enhance antitumor immunity by reshaping the tumor microenvironme
190 lopment of therapeutic strategies to enhance antitumor immunity by targeting myeloid cells as a colle
191 DCs, suggesting that exogenous DCs stimulate antitumor immunity by transferring antigens (Ags) to end
193 subsets results in superior persistence and antitumor immunity compared with ACT of populations cont
196 ent DCs are critical determinants for T cell antitumor immunity, effector T cell trafficking to the t
198 he role of LGP2 in mediating DC function and antitumor immunity elicited by radiotherapy remains uncl
199 contributions of innate immune effectors to antitumor immunity, especially in the context of combina
200 f long-term antigen-specific T-cell-mediated antitumor immunity following intrathymic injection of pr
201 rapy as a viable approach to induce systemic antitumor immunity from a single localized injection.
203 ate a crucial role for interleukin (IL)-9 in antitumor immunity generated by the GITR agonistic antib
205 The critical role of PD-L1 in obstructing antitumor immunity has been demonstrated in multiple ani
206 f protumorigenic M2 macrophages and promotes antitumor immunity, highlighting an investigational ther
207 naive T cell subset enhances persistence and antitumor immunity; however, the majority of clinical st
208 gen processing, CD8 T-cell cytotoxicity, and antitumor immunity, identifying NURF as a candidate ther
209 ity, but secondary tumors were refractory to antitumor immunity if rechallenge occurred during the re
210 , TSC1-deficient iNKT cells display enhanced antitumor immunity in a melanoma lung metastasis model.
213 on nontumor cells is critical for inhibiting antitumor immunity in B16 melanoma and a genetically eng
217 ay exert a functional and clinical impact on antitumor immunity in cetuximab-treated individuals.
218 Hodgkin Reed-Sternberg (HRS) cells to evade antitumor immunity in classical Hodgkin lymphoma (cHL).
224 ocyte-associated protein 4 (CTLA-4) restored antitumor immunity in miR-155 T cell-conditional KO mice
226 tibodies that block these receptors increase antitumor immunity in patients with melanoma, non-small-
228 antagonists are also accompanied by enhanced antitumor immunity in PD-L1-expressing triple-negative b
229 pigenetic silencing in tumor progression and antitumor immunity in primary cutaneous anaplastic T-cel
230 ne profiling suggested enhanced systemic and antitumor immunity in responding patients with a favorab
231 ablation of eosinophils severely compromises antitumor immunity in syngeneic and genetic models of co
232 ental inflammatory stimuli can contribute to antitumor immunity in the absence of cognate Ag recognit
236 we show that its targeting in mice enhances antitumor immunity in two syngeneic models of cancer.
237 regulate cancer-associated inflammation and antitumor immunity, in particular, the interactions betw
238 were associated with increased expression of antitumor immunity, including activation of CD8-positive
243 Although it is now widely appreciated that antitumor immunity is critical to impede tumor growth an
246 h detrimental (autoimmunity) and beneficial (antitumor immunity), it is vital to understand how ubiqu
247 of natural killer (NK) cell-mediated innate antitumor immunity, leading to increased lung metastases
248 radiation on priming and effector phases of antitumor immunity make it an appealing strategy to gene
249 tion, copriming with CD4(+) T cells improved antitumor immunity mediated by higher avidity, melanoma-
250 vaccine that allows simultaneous analysis of antitumor immunity mediated by transferred and endogenou
251 an immunodeficient animal model and augments antitumor immunity of CD8 T cells in a mouse model of ce
252 nt cytotoxicity in radiation therapy-induced antitumor immunity, proposing SLC7A2 as a new putative p
256 riers to effective drug delivery and promote antitumor immunity.See related commentary by Huang and B
257 utic benefits by augmenting NK cell-mediated antitumor immunity.Significance: Ablating adenosine sign
258 e results, which have implications for human antitumor immunity, suggest that TGF-beta targets T cell
259 e NK cells can be activated to contribute to antitumor immunity, supporting their potential as an imp
260 is defined by diminished CD8 T cell-mediated antitumor immunity that can respond to timely checkpoint
261 olymerase (PARP) inhibitors (PARPis) exhibit antitumor immunity that occurs in a stimulator of interf
262 stem cells (CSC) are known to suppress host antitumor immunity, the underlying mechanisms of which n
263 on strategy that achieves safe and effective antitumor immunity through in situ NK cell activation in
264 eficiency within CD4 Tregs leads to enhanced antitumor immunity through induction of an unstable phen
265 I), a new form of immunotherapy that elicits antitumor immunity through multiplexed activation of end
266 These results suggest that CXCL14 enacts antitumor immunity through restoration of MHC-I expressi
267 value of ERK5-targeted therapies to restore antitumor immunity through the blockade of protumorigeni
268 bicin can contribute to re-establishing host antitumor immunity through the generation of immunogenic
269 ivation, dendritic cell (DC) maturation, and antitumor immunity through the photoactivation of engine
270 n, which can potentially initiate or amplify antitumor immunity through the release of tumor-associat
273 licited by multiple 'targeted' inhibitors on antitumor immunity, underscoring the complex effects res
274 ere, we define the role of ICOS signaling in antitumor immunity using a blocking, nondepleting antibo
275 ired organ allograft tolerance and unleashed antitumor immunity via epigenetic activation of effector
278 nti-PD-L1, because it was assumed that their antitumor immunity was compromised compared with immunoc
282 T regulatory cells were nearly abolished and antitumor immunity was mediated by CD8 cytotoxic T lymph
284 with the goal of revealing their effects on antitumor immunity, we developed ARB nanoconjugates that
285 polarized macrophage populations in favor of antitumor immunity were not seen with checkpoint blockad
287 immunity and promoting tolerance to suppress antitumor immunity, whether and how pDCs cross-prime CD8
288 nsPEF restored but did not boost the natural antitumor immunity which stays dormant in the tumor-bear
289 e of the tumor landscape that contributes to antitumor immunity, which can be manipulated therapeutic
290 ent using tumor-specific mAbs can facilitate antitumor immunity, which could be augmented further wit
291 mote the development of a clinically desired antitumor immunity, which is known to promote favorable
292 cells (cDC1s) are required for antiviral and antitumor immunity, which necessitates an understanding
293 iota and observed differences in spontaneous antitumor immunity, which were eliminated upon cohousing
294 gram the tumor microenvironment and activate antitumor immunity while reducing the incidence of immun
295 enhanced T cell differentiation and impaired antitumor immunity, while Fas signaling blockade preserv
298 SYNB1891 treatment results in efficacious antitumor immunity with the formation of immunological m
299 50, an allosteric inhibitor of SHP2, induces antitumor immunity, with effects equivalent to or greate
300 2 polarization of TAMs and how TAMs suppress antitumor immunity within the tumor microenvironment (TM