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V-domain Ig suppressor of T cell activation (VISTA) is a transmembrane protein that plays a crucial role in the regulation of antitumor immunity. Therapeutic intervention that inhibits the VISTA pathway constitutes a new approach in the treatment of cancer. The aim of the present study was to provide a bibliometric literature review of VISTA resear...
Citations
... Targeting the VISTA protein, a V-domain Ig suppressor of T cell activation, is becoming increasingly important in cancer research because it has been proven to be an important immunological checkpoint and therapeutic target [16,17]. A significant number of immune cells express VISTA, which is associated with the control of immunity by controlling the immune response, including inhibition of T cell activation [16][17][18][19][20][21][22]. ...
... Targeting the VISTA protein, a V-domain Ig suppressor of T cell activation, is becoming increasingly important in cancer research because it has been proven to be an important immunological checkpoint and therapeutic target [16,17]. A significant number of immune cells express VISTA, which is associated with the control of immunity by controlling the immune response, including inhibition of T cell activation [16][17][18][19][20][21][22]. Recent research findings highlight some of the key aspects of VISTA's involvement in immune regulation and its potential as a target for cancer therapy. ...
A checkpoint protein called the V-domain Ig suppressor of T cell activation (VISTA) is important for controlling immune responses. Immune cells that interact with VISTA have molecules, or receptors, known as VISTA receptors. Immune system activity can be modified by the interaction between VISTA and its receptors. Since targeting VISTA or its receptors may be beneficial in certain conditions, VISTA has been studied in relation to immunotherapy for cancer and autoimmune illnesses. The purpose of this study was to examine the expression levels and interactions between VISTA and its receptors, VSIG3 and PSGL-1, in breast cancer tissues. IHC analysis revealed higher levels of proteins within the VISTA/VSIG3/PSGL-1 axis in cancer tissues than in the reference samples (mastopathies). VISTA was found in breast cancer cells and intratumoral immune cells, with membranous and cytoplasmic staining patterns. VISTA was also linked with pathological grade and VSIG3 and PSGL-1 levels. Furthermore, we discovered that the knockdown of one axis member boosted the expression of the other partners. This highlights the significance of VISTA/VSIG3/PSGL-1 in tumor stroma and microenvironment remodeling. Our findings indicate the importance of the VISTA/VSIG3/PSGL-1 axis in the molecular biology of cancer cells and the immune microenvironment.
... Thus, novel immunotherapy targets warrant further exploration. According to our review and bibliometric study, VISTA and its ligands, especially for IGSF11, may be the novel and promising target in tumor immunotherapy [110,111]. ...
Immunotherapy has become the major treatment for tumors in clinical practice, but some intractable problems such as the low response rate and high rates of immune-related adverse events still hinder the progress of tumor immunotherapy. Hence, it is essential to explore additional immunotherapy treatment targets. In this review, we focus on the structure, expression and expression-related mechanisms, interactions, biological functions and the progress in preclinical/clinical research of IGSF11 and VISTA in tumors. We cover the progress in recent research with this pair of immune checkpoints in tumor immune regulation, proliferation, immune resistance and predictive prognosis. Both IGSF11 and VISTA are highly expressed in tumors and are modulated by various factors. They co-participate in the functional regulation of immune cells and the inhibition of cytokine production. Besides, in the downregulation of IGSF11 and VISTA, both inhibit the growth of some tumors. Preclinical and clinical trials all emphasize the predictive role of IGSF11 and VISTA in the prognosis of tumors, and that the predictive role of the same gene varies from tumor to tumor. At present, further research is proving the enormous potential of IGSF11 and VISTA in tumors, and especially the role of VISTA in tumor immune resistance. This may prove to be a breakthrough to solve the current clinical immune resistance, and most importantly, since research has focused on VISTA but less on IGSF11, IGSF11 may be the next candidate for tumor immunotherapy.
... VISTA is another immune checkpoint that is crucial in regulating anti-tumoral immunity [3]. VISTA is a type I transmembrane molecule with a single N-terminal Ig V-domain, a stalk of approximately 30 amino acids, a transmembrane domain, and a 95-amino acid cytoplasmic tail. ...
Dendritic cells (DCs) can present tumoral antigens to T-cells and stimulate T-cell-mediated anti-tumoral immune responses. In addition to uptaking, processing, and presenting tumoral antigens to T-cells, co-stimulatory signals have to be established between DCs with T-cells to develop anti-tumoral immune responses. However, most of the tumor-infiltrated immune cells are immunosuppressive in the tumor microenvironment (TME), paving the way for immune evasion of tumor cells. This immunosuppressive TME has also been implicated in suppressing the DC-mediated anti-tumoral immune responses, as well. Various factors, i.e., immunoregulatory cells, metabolic factors, tumor-derived immunosuppressive factors, and inhibitory immune checkpoint molecules, have been implicated in developing the immunosuppressive TME. Herein, we aimed to review the biology of DCs in developing T-cell-mediated anti-tumoral immune responses, the significance of immunoregulatory cells in the TME, metabolic barriers contributing to DCs dysfunction in the TME, tumor-derived immunosuppressive factors, and inhibitory immune checkpoint molecules in DC-based cell therapy outcomes. With reviewing the ongoing clinical trials, we also proposed a novel therapeutic strategy to increase the efficacy of DC-based cell therapy. Indeed, the combination of DC-based cell therapy with monoclonal antibodies against novel immune checkpoint molecules can be a promising strategy to increase the response rate of patients with cancers.
