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1 ICB regulate overlapping pathways to promote antitumor immunity.
2 onstrated evidence of durable tumor-specific antitumor immunity.
3 he antigenic breadth and clonal diversity of antitumor immunity.
4 ying cancer cells that can incite protective antitumor immunity.
5 +) cells inhibits tumor growth by augmenting antitumor immunity.
6 by peptide vaccines and enhanced therapeutic antitumor immunity.
7 targeted for enhancing vaccine efficacy and antitumor immunity.
8 upts PD-1-mediated signaling and may restore antitumor immunity.
9 other strategies of Treg ablation to promote antitumor immunity.
10 hereas IFN-gamma production is essential for antitumor immunity.
11 immune responses and may have a key role in antitumor immunity.
12 be exploited to generate a more efficacious antitumor immunity.
13 dies can lead to tumor clearance and durable antitumor immunity.
14 ng and selective subset expansion to restore antitumor immunity.
15 associated DC function to support or enhance antitumor immunity.
16 ng effective vaccine induction of protective antitumor immunity.
17 development of multivalent DLL1 to stimulate antitumor immunity.
18 nment is known to inhibit effective adaptive antitumor immunity.
19 role in regulating tumor immunogenicity and antitumor immunity.
20 th 1 is an immune checkpoint that suppresses antitumor immunity.
21 not required for vitiligo or its associated antitumor immunity.
22 n a manner associated with enhanced systemic antitumor immunity.
23 une activation can induce local and systemic antitumor immunity.
24 the immunological synapse in T cell-mediated antitumor immunity.
25 D47-SIRPalpha axis is critical for DC-driven antitumor immunity.
26 nce for its beneficial role in antiviral and antitumor immunity.
27 hocytes that play key roles in antiviral and antitumor immunity.
28 iated with activation of potent and specific antitumor immunity.
29 and minimal residual disease for generating antitumor immunity.
30 1 and AdipoR2, which are sufficient to blunt antitumor immunity.
31 essive Tregs or MDSCs, resulting in enhanced antitumor immunity.
32 n, as inhibition of STAT3 signaling enhances antitumor immunity.
33 , thus preventing the development of durable antitumor immunity.
34 rug in its ability to productively stimulate antitumor immunity.
35 e development of Th17 cells and impacting on antitumor immunity.
36 hematopoietic cells and enhances protective antitumor immunity.
37 induced responses are inadequate to maintain antitumor immunity.
38 agents, antiangiogenic effects, and altering antitumor immunity.
39 t the same time potently stimulating NK cell antitumor immunity.
40 ess malignant growth and stimulate long-term antitumor immunity.
41 ntions against this pathway can help restore antitumor immunity.
42 of immune cells are essential for effective antitumor immunity.
43 mmunogenic MC38 tumor cells allows effective antitumor immunity.
44 Human NK lymphocytes are involved in antitumor immunity.
45 rvival conferred by sustained NKG2D-mediated antitumor immunity.
46 f Gfi1 in this process, loss of Gfi1 dampens antitumor immunity.
47 sion of regulatory T cells, which dampen the antitumor immunity.
48 eceptors previously correlated with improved antitumor immunity.
49 hanism of sMIC-induced impairment of NK cell antitumor immunity.
50 cells (MDSC), which inhibit host protective antitumor immunity.
51 of miR-155 in T cells, in which it promotes antitumor immunity.
52 emokine CXCL9/Mig, an important component of antitumor immunity.
53 1) and its receptor (CX3CR1) are involved in antitumor immunity.
54 d to trigger tumor cell apoptosis or enhance antitumor immunity.
55 and plays an important role in antiviral and antitumor immunity.
56 anti-CD137 (4-1BB) mAbs enhance CD8-mediated antitumor immunity.
57 is thought to contribute to the dampening of antitumor immunity.
58 s to the induction of CD8(+) T cell-mediated antitumor immunity.
59 ukemia-reactive T cells and thereby enhances antitumor immunity.
60 ted Treg infiltration and the suppression of antitumor immunity.
61 DCs are features of successful activation of antitumor immunity.
62 agues report a central role for Th9 cells in antitumor immunity.
63 aying an important role in antimicrobial and antitumor immunity.
64 s underlying melanoma progression as well as antitumor immunity.
65 T-cell expansion/accumulation and protective antitumor immunity.
66 n of established melanomas and generation of antitumor immunity.
67 nselected tumor cells in inducing protective antitumor immunity.
68 links oncogenic activation to the evasion of antitumor immunity.
69 se of proinflammatory cytokines that promote antitumor immunity.
70 pecific immune responses, such as sepsis and antitumor immunity.
71 ng in the collateral limitation of efficient antitumor immunity.
72 egarded as an attractive strategy to enhance antitumor immunity.
73 is known regarding the impact of obesity on antitumor immunity.
74 ammatory effects of TLR ligands that support antitumor immunity.
75 eting strategies may also enhance allogeneic antitumor immunity.
76 levels of FAP-alpha, a crucial suppressor of antitumor immunity.
77 e of selective targeting CSCs and conferring antitumor immunity.
78 mor PD-L1 is not just a marker of suppressed antitumor immunity.
79 In preclinical models, it contributes to antitumor immunity.
80 development on the basis of their effect on antitumor immunity.
81 disseminating tumor cells from NK-dependent antitumor immunity.
82 o promote antitumor responses by reinforcing antitumor immunity.
83 NKT (iNKT) cell adjuvant activity and boost antitumor immunity.
84 ting SRA/CD204 strongly enhances DC-mediated antitumor immunity.
85 iological fusion protein to induce effective antitumor immunity.
86 antigens and for the induction of long-term antitumor immunity.
87 e the generation of both acute and long-term antitumor immunity.
88 ance could lead to new strategies to enhance antitumor immunity.
89 icit poorly understood effects on protective antitumor immunity.
90 overcoming TGF-beta1-induced suppression of antitumor immunity.
91 article formulation of doxorubicin, enhances antitumor immunity.
92 he former of which are superior in mediating antitumor immunity.
93 pansion reduces memory potential and impairs antitumor immunity.
94 induce long-lasting CD8(+) T cell-dependent antitumor immunity.
95 s, driven by cytotoxic T-lymphocyte-mediated antitumor immunity.
96 f Th1-mediated and cytotoxic T-cell-mediated antitumor immunity.
97 equently amplify immune response to systemic antitumor immunity.
98 or reversing immunosuppression and enhancing antitumor immunity.
99 ergy and tumor defense, where it can promote antitumor immunity.
100 sociated sialosides may therefore potentiate antitumor immunity.
101 into T effector cells and leads to enhanced antitumor immunity.
102 thways responsible for the downregulation of antitumor immunity.
103 ll activation and promotion of CD8(+) T cell antitumor immunity.
104 neoantigen intratumor heterogeneity (ITH) on antitumor immunity.
105 ng, and ultimately depended on CD8(+) T cell antitumor immunity.
106 a serious candidate for the reactivation of antitumor immunity.
107 ated in the nMOF channels to induce systemic antitumor immunity.
108 kdown of human EZH2 in T cells elicited poor antitumor immunity.
109 n the presence of spontaneous or therapeutic antitumor immunity.
110 ), the inhibition of which results in potent antitumor immunity.
111 crucial for in situ MDA-5-induced protective antitumor immunity.
112 onment that might blunt the effectiveness of antitumor immunity.
113 vessel paradigm and discuss its relevance to antitumor immunity.
114 as a candidate therapeutic target to enhance antitumor immunity.
115 comes, credited to their ability to suppress antitumor immunity.
116 cule that limits autoimmunity, antiviral and antitumor immunity.
117 ts tumor-derived DNA and generates intrinsic antitumor immunity.
118 ells (cDCs) is important in host defense and antitumor immunity.
119 hence, they play a role in antimicrobial and antitumor immunity.
120 ctivate a patient's immune system to unleash antitumor immunity.
121 rapeutic costimulatory signaling and restore antitumor immunity.
122 rtain contexts, have an inhibitory effect on antitumor immunity, a finding with implications for immu
123 documented a marked increase in the level of antitumor immunity achieved against established B16 tumo
124 ever, the critical determinants of effective antitumor immunity after chemotherapy have not been defi
125 f Ad.E6E7.p16 with Ad.alphaPD1 could improve antitumor immunity against HPV-related tumors and that p
126 he myeloid cell response was used to mediate antitumor immunity against melanoma tumors (with less de
127 with AP1903 in vaccinated mice led to robust antitumor immunity against preestablished E.G7-OVA lymph
128 tin (TSLP) at a distant site leads to robust antitumor immunity against spontaneous breast carcinogen
129 a tumor-specific antibody fails to generate antitumor immunity against syngeneic B16F10 tumors in mi
130 mmunotherapy is potent to enhance the host's antitumor immunity against uveal melanoma in approximate
131 ancer cells into the circulation, suppresses antitumor immunity allowing circulating cells to survive
133 sive tumors to secrete galectin-1, dampening antitumor immunity and accelerating malignant progressio
134 immunotherapies are urgently needed to boost antitumor immunity and control disease in cancer patient
135 vasculature in the initiation of CD8 T-cell antitumor immunity and demonstrate that tumor endothelia
136 ey mechanism by which tumor PD-L1 suppresses antitumor immunity and demonstrate that tumor PD-L1 is n
137 eviews the mechanisms by which PD-L1 impairs antitumor immunity and discusses established and experim
138 cal to elucidating the role of Th17 cells in antitumor immunity and for the design of novel therapeut
139 established for chronic viral infection and antitumor immunity and has been found to be associated w
142 udies have shown that OX40 agonists increase antitumor immunity and improve tumor-free survival.
143 show that blockade of Fas signaling enhances antitumor immunity and increases survival in a mouse mod
144 fic Th9 cells in provoking CD8+ CTL-mediated antitumor immunity and indicate that Th9 cell-based canc
145 -ligand 1 (PD-L1) immune checkpoint augments antitumor immunity and induces durable responses in pati
146 hat, in mice, gut commensal microbes promote antitumor immunity and may determine therapy efficacy.
147 ative pathway for DC/NK cell interactions in antitumor immunity and may reflect homeostasis of both D
148 ings aid in deciphering the role for pDCs in antitumor immunity and present a promising prospect of d
154 on therapy with CTLA-4 blockade will augment antitumor immunity and rejection of tumor metastases in
155 in the understanding of basic principles of antitumor immunity and strategies for increasing the suc
156 s might be a novel mechanism for suppressing antitumor immunity and supporting tumor growth through t
157 nistic CD40 antibody was sufficient to evoke antitumor immunity and suppress tumor growth in tumor-be
158 administration of 3M-052 generated systemic antitumor immunity and suppressed both injected and dist
159 the cGAS pathway is important for intrinsic antitumor immunity and that cGAMP may be used directly f
161 trating leukocytes (TILeus) induces systemic antitumor immunity and tumor regression, but not in TME
162 fore considered promising targets to enhance antitumor immunity, and approaches for their therapeutic
163 opment of allospecific transplant tolerance, antitumor immunity, and cross-generational reproductive
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
169 noclonal antibody (mAb) drugs that stimulate antitumor immunity are transforming cancer treatment but
171 enocarcinoma cells is sufficient to suppress antitumor immunity, as deletion of PD-L1 on highly immun
172 e investigations of early stages of adaptive antitumor immunity, as well as support the rationale for
173 7 homolog 1 or CD274) is a major obstacle to antitumor immunity because it tolerizes/anergizes tumor-
174 ial for these cells to "jump-start" adaptive antitumor immunity before their elimination by host allo
175 ive regulatory T cells (Treg cells) suppress antitumor immunity, but how Treg cells behave in the met
176 immune blockades in tumors limits successful antitumor immunity, but the mechanisms underlying this p
177 suppression within the tumor, and reactivate antitumor immunity, but they have yet to live up to thei
179 okines induces a potent antitumor effect and antitumor immunity by ameliorating the immunosuppressive
182 the stromal extracellular matrix influences antitumor immunity by controlling the positioning and mi
183 CD47 in the context of radiotherapy enhances antitumor immunity by directly stimulating CD8(+) cytoto
184 emonstrate that GITR co-stimulation mediates antitumor immunity by promoting TH9 cell differentiation
185 identified as a potential target to modulate antitumor immunity by reversing MDSC-mediated immunosupp
186 ria toxin, was initially expected to enhance antitumor immunity by selectively eliminating regulatory
187 lopment of therapeutic strategies to enhance antitumor immunity by targeting myeloid cells as a colle
190 subsets results in superior persistence and antitumor immunity compared with ACT of populations cont
191 g-specific CD8+ T cells in vivo and improved antitumor immunity compared with that observed with DCs
192 lymph node(s), effective local and systemic antitumor immunity could be achieved in the absence of s
195 ent DCs are critical determinants for T cell antitumor immunity, effector T cell trafficking to the t
197 lls (pDCs) have a crucial role in triggering antitumor immunity especially in melanoma, we explored t
198 contributions of innate immune effectors to antitumor immunity, especially in the context of combina
199 f long-term antigen-specific T-cell-mediated antitumor immunity following intrathymic injection of pr
200 ate a crucial role for interleukin (IL)-9 in antitumor immunity generated by the GITR agonistic antib
202 The critical role of PD-L1 in obstructing antitumor immunity has been demonstrated in multiple ani
204 ntly uncovered role for host type I IFNs for antitumor immunity has important fundamental and clinica
205 A link between autoimmunity and improved antitumor immunity has long been recognized, although th
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
215 ponses underlie the development of effective antitumor immunity in BR mice and the lack thereof in PE
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 We show here that fundamental aspects of antitumor immunity in mice are significantly influenced
225 ocyte-associated protein 4 (CTLA-4) restored antitumor immunity in miR-155 T cell-conditional KO mice
227 tibodies that block these receptors increase antitumor immunity in patients with melanoma, non-small-
228 pigenetic silencing in tumor progression and antitumor immunity in primary cutaneous anaplastic T-cel
229 ne profiling suggested enhanced systemic and antitumor immunity in responding patients with a favorab
230 ucible genes involved in innate and adaptive antitumor immunity in spite of elevated levels of NF-kap
231 that BiTEs can be used to elicit functional antitumor immunity in the CNS, and that peptide blockade
232 T cells act as the "gatekeepers" of the host antitumor immunity in the postchemotherapy setting, ther
233 we show that its targeting in mice enhances antitumor immunity in two syngeneic models of cancer.
234 were associated with increased expression of antitumor immunity, including activation of CD8-positive
236 ata raise the hypothesis that suppression of antitumor immunity is an outcome of cold stress-induced
238 Although it is now widely appreciated that antitumor immunity is critical to impede tumor growth an
239 to one that is favorable to the induction of antitumor immunity is indispensable for effective cancer
244 trast, many genes frequently associated with antitumor immunity lack STAT3 DNA-binding site(s) and ca
245 radiation on priming and effector phases of antitumor immunity make it an appealing strategy to gene
246 pressive environment while activating innate antitumor immunity may be an effective approach to cance
247 tion, copriming with CD4(+) T cells improved antitumor immunity mediated by higher avidity, melanoma-
248 entiation into memory T cells and potentiate antitumor immunity more effectively than the pharmacolog
249 an immunodeficient animal model and augments antitumor immunity of CD8 T cells in a mouse model of ce
251 erving conversion to donor hematopoiesis and antitumor immunity, providing a rationale for exploring
256 +) T cells to control infections and mediate antitumor immunity requires the development and survival
257 n 8-gene Tfh signature, signifying organized antitumor immunity, robustly predicted survival or preop
258 utic benefits by augmenting NK cell-mediated antitumor immunity.Significance: Ablating adenosine sign
259 highly effective in mobilizing or restoring antitumor immunity, supporting the potential therapeutic
260 ts and impaired class II-restricted auto and antitumor immunity that could be rescued by supplemental
261 ctive antitumor memory and elicited systemic antitumor immunity that significantly inhibited the grow
263 oth Tc1 and Tc17 cells can mediate effective antitumor immunity through distinct effector mechanisms,
264 eficiency within CD4 Tregs leads to enhanced antitumor immunity through induction of an unstable phen
266 bicin can contribute to re-establishing host antitumor immunity through the generation of immunogenic
267 ivation, dendritic cell (DC) maturation, and antitumor immunity through the photoactivation of engine
268 n, which can potentially initiate or amplify antitumor immunity through the release of tumor-associat
269 nhance or limit DC responses associated with antitumor immunity, through their relative ability to in
270 ts indicate that booster vaccinations impact antitumor immunity to different extents, depending on th
272 Cells acquiring gp96 can transfer protective antitumor immunity to naive mice by actively cross-prese
273 alignancy by initiating or reactivating host antitumor immunity to otherwise poorly immunogenic and i
274 ic inflammation that combines with defective antitumor immunity to promote lung tumor formation, repr
275 licited by multiple 'targeted' inhibitors on antitumor immunity, underscoring the complex effects res
276 ere, we define the role of ICOS signaling in antitumor immunity using a blocking, nondepleting antibo
277 s study, we investigated the role of BLT1 in antitumor immunity using syngeneic TC-1 cervical cancer
278 uggest the successful activation of systemic antitumor immunity using this approach in this specific
279 lceramide (alpha-GalCer) in animals enhances antitumor immunity via activation of the invariant NKT (
282 nti-PD-L1, because it was assumed that their antitumor immunity was compromised compared with immunoc
287 cells also secreted IFN-gamma, Tc17-mediated antitumor immunity was independent of the direct effects
289 T regulatory cells were nearly abolished and antitumor immunity was mediated by CD8 cytotoxic T lymph
291 ortance of this NK cell subset for effective antitumor immunity was shown by adoptively transferring
292 dritic cells (DC) are critical regulators of antitumor immunity, we examined the combined effects of
294 nsplantation recipients results in increased antitumor immunity when adoptively transferred T cells a
295 e that nondominant CD8(+) T cells can induce antitumor immunity when combined with regulatory T cell-
296 ent using tumor-specific mAbs can facilitate antitumor immunity, which could be augmented further wit
297 mote the development of a clinically desired antitumor immunity, which is known to promote favorable
298 iota and observed differences in spontaneous antitumor immunity, which were eliminated upon cohousing
299 enhanced T cell differentiation and impaired antitumor immunity, while Fas signaling blockade preserv
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