dc.creator | Vetsika E.-K., Koukos A., Kotsakis A. | en |
dc.date.accessioned | 2023-01-31T10:32:53Z | |
dc.date.available | 2023-01-31T10:32:53Z | |
dc.date.issued | 2019 | |
dc.identifier | 10.3390/cells8121647 | |
dc.identifier.issn | 20734409 | |
dc.identifier.uri | http://hdl.handle.net/11615/80606 | |
dc.description.abstract | Myeloid-derived suppressor cells (MDSCs) constitute a vast population of immature myeloid cells implicated in various conditions. Most notably, their role in cancer is of great complexity. They exert immunosuppressive functions like hampering cancer immunity mediated by T lymphocytes and natural killer cells, while simultaneously they can recruit T regulatory cells to further promote immunosuppression, thus shielding tumor cells against the immune defenses. In addition, they were shown to support tumor invasion and metastasis by inducing vascularization. Yet again, in order to exert their angiogenic activities, they do have at their disposal a variety of occasionally overlapping mechanisms, mainly driven by VEGF/JAK/STAT signaling. In this concept, they have risen to be a rather attractive target for therapies, including depletion or maturation, so as to overcome cancer immunity and suppress angiogenic activity. Even though, many studies have been conducted to better understand these cells, there is much to be done yet. This article hopes to shed some light on the paradoxal complexity of these cells, while elucidating some of the key features of MDSCs in relation to immunosuppression and, most importantly, to the vascularization processes, along with current therapeutic options in cancer, in relation to MDSC depletion. © 2019 by the authors. Licensee MDPI, Basel, Switzerland. | en |
dc.language.iso | en | en |
dc.source | Cells | en |
dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85084367313&doi=10.3390%2fcells8121647&partnerID=40&md5=8c26041b9f7592b00995db1b44f9f68c | |
dc.subject | antineoplastic agent | en |
dc.subject | arginase 1 | en |
dc.subject | atezolizumab | en |
dc.subject | bevacizumab | en |
dc.subject | capecitabine | en |
dc.subject | carboplatin | en |
dc.subject | CCAAT enhancer binding protein epsilon | en |
dc.subject | dendritic cell vaccine | en |
dc.subject | docetaxel | en |
dc.subject | gemcitabine | en |
dc.subject | granulocyte colony stimulating factor | en |
dc.subject | granulocyte macrophage colony stimulating factor | en |
dc.subject | heat shock protein 72 | en |
dc.subject | high mobility group B1 protein | en |
dc.subject | hypoxia inducible factor 1alpha | en |
dc.subject | imiquimod | en |
dc.subject | immunoglobulin enhancer binding protein | en |
dc.subject | inducible nitric oxide synthase | en |
dc.subject | interferon consensus sequence binding protein | en |
dc.subject | ipilimumab | en |
dc.subject | Janus kinase | en |
dc.subject | matrix metalloproteinase | en |
dc.subject | nivolumab | en |
dc.subject | pembrolizumab | en |
dc.subject | pemetrexed | en |
dc.subject | rgx 104 | en |
dc.subject | STAT protein | en |
dc.subject | unclassified drug | en |
dc.subject | unindexed drug | en |
dc.subject | vasculotropin | en |
dc.subject | vinorelbine tartrate | en |
dc.subject | histone deacetylase inhibitor | en |
dc.subject | vasculotropin receptor | en |
dc.subject | angiogenesis | en |
dc.subject | antiangiogenic therapy | en |
dc.subject | antigen presenting cell | en |
dc.subject | cancer therapy | en |
dc.subject | CD4+ T lymphocyte | en |
dc.subject | CD8+ T lymphocyte | en |
dc.subject | cytokine production | en |
dc.subject | down regulation | en |
dc.subject | exosome | en |
dc.subject | glioblastoma | en |
dc.subject | human | en |
dc.subject | immune deficiency | en |
dc.subject | immunosuppressive treatment | en |
dc.subject | lymphoma | en |
dc.subject | myeloid-derived suppressor cell | en |
dc.subject | natural killer cell | en |
dc.subject | neoplasm | en |
dc.subject | non small cell lung cancer | en |
dc.subject | nonhuman | en |
dc.subject | nuclear reprogramming | en |
dc.subject | phase 1 clinical trial (topic) | en |
dc.subject | phase 2 clinical trial (topic) | en |
dc.subject | phenotype | en |
dc.subject | protein expression | en |
dc.subject | regulatory T lymphocyte | en |
dc.subject | Review | en |
dc.subject | sarcoma | en |
dc.subject | signal transduction | en |
dc.subject | systematic review | en |
dc.subject | Th17 cell | en |
dc.subject | tumor associated leukocyte | en |
dc.subject | tumor cell destruction | en |
dc.subject | tumor immunity | en |
dc.subject | tumor invasion | en |
dc.subject | upregulation | en |
dc.subject | vascularization | en |
dc.subject | bone marrow cell | en |
dc.subject | immunological tolerance | en |
dc.subject | immunology | en |
dc.subject | immunosuppressive treatment | en |
dc.subject | metabolism | en |
dc.subject | myeloid-derived suppressor cell | en |
dc.subject | neoplasm | en |
dc.subject | pathology | en |
dc.subject | physiology | en |
dc.subject | T lymphocyte | en |
dc.subject | tumor microenvironment | en |
dc.subject | Histone Deacetylase Inhibitors | en |
dc.subject | Humans | en |
dc.subject | Immune Tolerance | en |
dc.subject | Immunosuppression | en |
dc.subject | Killer Cells, Natural | en |
dc.subject | Myeloid Cells | en |
dc.subject | Myeloid-Derived Suppressor Cells | en |
dc.subject | Neoplasms | en |
dc.subject | Neovascularization, Physiologic | en |
dc.subject | Receptors, Vascular Endothelial Growth Factor | en |
dc.subject | Signal Transduction | en |
dc.subject | T-Lymphocytes | en |
dc.subject | Tumor Microenvironment | en |
dc.subject | MDPI | en |
dc.title | Myeloid-derived suppressor cells: Major figures that shape the immunosuppressive and angiogenic network in cancer | en |
dc.type | other | en |