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The Role of V-Domain Ig Suppressor of T Cell Activation (VISTA) in Cancer Therapy: Lessons Learned and the Road Ahead.

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TLDR
Wang et al. as mentioned in this paper reviewed the current evidence about the structure and expression pattern of VISTA, its role in TME, the clinicopathological significance, and its prognostic values in various cancers and proposed a strategy to overcome tumor immune-resistance states.
Abstract
Immune checkpoints (ICs) have pivotal roles in regulating immune responses. The inhibitory ICs in the tumor microenvironment (TME) have been implicated in the immune evasion of tumoral cells. Therefore, identifying and targeting these inhibitory ICs might be critical for eliminating tumoral cells. V-domain immunoglobulin suppressor of T cell activation (VISTA) is a novel inhibitory IC that is expressed on myeloid cells, lymphoid cells, and tumoral cells; therefore, VISTA can substantially regulate innate and adaptive anti-tumoral immune responses. Besides, growing evidence indicates that VISTA blockade can enhance the sensitivity of tumoral cells to conventional IC-based immunotherapy, e.g., cytotoxic T lymphocyte antigen 4 (CTLA-4) inhibitors. In this regard, the current study aimed to review the current evidence about the structure and expression pattern of VISTA, its role in TME, the clinicopathological significance of VISTA, and its prognostic values in various cancers. Besides, this review intended to collect the lessons from the recent pre-clinical and clinical studies and propose a strategy to overcome tumor immune-resistance states.

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Dendritic cell-based cancer immunotherapy in the era of immune checkpoint inhibitors: From bench to bedside.

TL;DR: In this paper , the authors reviewed the biology of Dendritic cells in developing T-cell-mediated anti-tumoral immune responses, the significance of immunoregulatory cells in the tumor microenvironment, metabolic barriers contributing to DCs dysfunction in the TME, tumor-derived immunosuppressive factors, and inhibitory immune checkpoint molecules in DC-based cell therapy outcomes.
Journal ArticleDOI

Current Progress and Future Perspectives of Immune Checkpoint in Cancer and Infectious Diseases

TL;DR: In this paper, the authors reviewed the role of immune checkpoint inhibitors in clinical therapy of cancer and other diseases, and discussed the correlation between immune checkpoints and microorganisms and the role in microbial-infection diseases.
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Immune Checkpoint Inhibitors for Vaccine Improvements: Current Status and New Approaches

TL;DR: The current state and future directions of the use of ICIs in experimental and clinical settings, including mAbs and alternative new approaches using antisense oligonucleotides (ASOs), small non-coding RNAs, aptamers, peptides, and other small molecules for improving vaccine efficacy are reviewed.
References
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Journal ArticleDOI

The blockade of immune checkpoints in cancer immunotherapy

TL;DR: Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses.
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Immunity, Inflammation, and Cancer

TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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The future of immune checkpoint therapy

TL;DR: The way forward for this class of novel agents lies in the ability to understand human immune responses in the tumor microenvironment, which will provide valuable information regarding the dynamic nature of the immune response and regulation of additional pathways that will need to be targeted through combination therapies to provide survival benefit for greater numbers of patients.
Journal ArticleDOI

CTLA-4 can function as a negative regulator of T cell activation

TL;DR: Results suggest that the MAb may obstruct the interaction of CTLA-4 with its natural ligand and block a negative signal, or directly signal T cells to down-regulate immune function.
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