Silencing B7-H1 enhances the anti-tumor effect of bladder cancer antigen-loaded dendritic cell vaccine in vitro

Wang, Shuo; Wang, Yonghua; Liu, Jing; Shao, Shixiu; Li, Xianjun; Gao, Jiannan; Niu, Haitao; Wang, Xinsheng

doi:10.2147/ott.s65367

Cited by 16 publications

(12 citation statements)

References 24 publications

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“…Advanced clinical trials with PD-1 and PD-L1 antibodies show very promising results in preventing axis signaling in non-small cell lung cancer, indicating the potential that blocking this pathway enhances anti-tumor immunity ( 112 ). Silencing of PD-L1, on its own ( 113 ) or in combination with its phagocyte-restricted relative PD-L2 ( 114 ), shows augmented ex vivo TAA-specific CTL responses, which is also confirmed in vivo ( 115 ). Moreover, combined silencing of PD-L1 and IL-10 in DC vaccination showed even stronger induction of anti-tumor responses in vitro and in vivo ( 106 ) indicating the potential of combining DC modifications in maximizing anti-tumor responses.…”

Section: Interferance With Co-inhibitory and Immunosuppressive Pathwamentioning

confidence: 81%

Strategies to Genetically Modulate Dendritic Cells to Potentiate Anti-Tumor Responses in Hematologic Malignancies

et al. 2018

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Dendritic cell (DC) vaccination has been investigated as a potential strategy to target hematologic malignancies, while generating sustained immunological responses to control potential future relapse. Nonetheless, few clinical trials have shown robust long-term efficacy. It has been suggested that a combination of surmountable shortcomings, such as selection of utilized DC subsets, DC loading and maturation strategies, as well as tumor-induced immunosuppression may be targeted to maximize anti-tumor responses of DC vaccines. Generation of DC from CD34+ hematopoietic stem and progenitor cells (HSPCs) may provide potential in patients undergoing allogeneic HSPC transplantations for hematologic malignancies. CD34+ HSPC from the graft can be genetically modified to optimize antigen presentation and to provide sufficient T cell stimulatory signals. We here describe beneficial (gene)-modifications that can be implemented in various processes in T cell activation by DC, among which major histocompatibility complex (MHC) class I and MHC class II presentation, DC maturation and migration, cross-presentation, co-stimulation, and immunosuppression to improve anti-tumor responses.

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Section: Interferance With Co-inhibitory and Immunosuppressive Pathwamentioning

confidence: 81%

Strategies to Genetically Modulate Dendritic Cells to Potentiate Anti-Tumor Responses in Hematologic Malignancies

et al. 2018

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“…The possibility of such inconclusive studies have been checked so far because of a shortage of convincing evidence. 40 , 41 Maybe future work will be influenced by the decrease of match detection. By adding sampling rate and specific groups to prove gene, polymorphism and environmental factor will have an influence on morbidity of bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

Risks on N-acetyltransferase 2 and bladder cancer: a meta-analysis

Zhu¹,

Zhang²,

Jiang³

et al. 2015

OTT

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BackgroundIt is known that bladder cancer disease is closely related to aromatic amine compounds, which could cause cancer by regulating of N-acetylation and N-acetyltransferase 1 and 2 (NAT1 and NAT2). The NAT2 slowed acetylation and would increase the risk of bladder cancer, with tobacco smoke being regarded as a risk factor for this increased risk. However, the relationship between NAT2 slow acetylation and bladder cancer is still debatable at present. This study aims to explore preliminarily correlation of NAT2 slow acetylation and the risk of bladder cancer.MethodsThe articles were searched from PubMed, Cochran, McGrane English databases, CBM, CNKI, and other databases. The extraction of bladder cancer patients and a control group related with the NAT2 gene were detected by the state, and the referenced articles and publications were also used for data retrieval. Using a random effects model, the model assumes that the studies included in the analysis cases belong to the overall population in the study of random sampling, and considering the variables within and between studies. Data were analyzed using STATA Version 6.0 software, using the META module. According to the inclusion and exclusion criteria of the literature study, 20 independent studies are included in this meta-analysis.ResultsThe results showed that the individual differences of bladder cancer susceptibility might be part of the metabolism of carcinogens. Slow acetylation status of bladder cancer associated with the pooled odds ratio was 1.31 (95% confidence interval: 1.11–1.55).ConclusionThe status of NAT2 slow N-acetylation is associated with bladder cancer risks, and may increase the risk of bladder cancer.

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“…Focusing on the PD-1/PD-L pathway, silencing of PD-L1 and/or PD-L2 in DCs has been evaluated with different RNAi introduction techniques, including viral transduction and non-integrating electrotransfection, lipid nanoparticle transfection, and the cGMP-compliant transfection reagent SAINT-RED ( 77 , 138 , 141 , 143 , 144 ). Preclinical data demonstrated that PD-L-silenced DCs could (1) increase expansion, promote pro-inflammatory cytokine secretion and degranulation, and augment antitumor function of antigen-specific CD8 + T cells in human in vitro models ( 138 , 140 , 142 ) and (2) induce significant antitumor immunity in vivo in different malignant mouse models ( 139 , 141 ). Alternatively, in situ PD-L silencing can also be achieved through the use of small molecules.…”

Section: Strategies To Leverage DC Immunopotency By Interceding Pd-1/mentioning

confidence: 99%

Dendritic Cells and Programmed Death-1 Blockade: A Joint Venture to Combat Cancer

et al. 2018

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Two decades of clinical cancer research with dendritic cell (DC)-based vaccination have proved that this type of personalized medicine is safe and has the capacity to improve survival, but monotherapy is unlikely to cure the cancer. Designed to empower the patient’s antitumor immunity, huge research efforts are set to improve the efficacy of next-generation DC vaccines and to find synergistic combinations with existing cancer therapies. Immune checkpoint approaches, aiming to breach immune suppression and evasion to reinforce antitumor immunity, have been a revelation in the immunotherapy field. Early success of therapeutic antibodies blocking the programmed death-1 (PD-1) pathway has sparked the development of novel inhibitors and combination therapies. Hence, merging immunoregulatory tumor-specific DC strategies with PD-1-targeted approaches is a promising path to explore. In this review, we focus on the role of PD-1-signaling in DC-mediated antitumor immunity. In the quest of exploiting the full potential of DC therapy, different strategies to leverage DC immunopotency by impeding PD-1-mediated immune regulation are discussed, including the most advanced research on targeted therapeutic antibodies, lessons learned from chemotherapy-induced immune activation, and more recent developments with soluble molecules and gene-silencing techniques. An overview of DC/PD-1 immunotherapy combinations that are currently under preclinical and clinical investigation substantiates the clinical potential of such combination strategies.

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Silencing B7-H1 enhances the anti-tumor effect of bladder cancer antigen-loaded dendritic cell vaccine in vitro

Cited by 16 publications

References 24 publications

Strategies to Genetically Modulate Dendritic Cells to Potentiate Anti-Tumor Responses in Hematologic Malignancies

Strategies to Genetically Modulate Dendritic Cells to Potentiate Anti-Tumor Responses in Hematologic Malignancies

Risks on N-acetyltransferase 2 and bladder cancer: a meta-analysis

Dendritic Cells and Programmed Death-1 Blockade: A Joint Venture to Combat Cancer

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