Tumor-derived factors affecting immune cells. (August 2017)

• Record Type: Journal Article
• Authors: Russo, Vincenzo; Protti, Maria Pia
• Is Part Of: Cytokine & growth factor reviews. Volume 36(2017)
• Page Start: 79
• Page End: 87
• Publication Date: 2017-08
• Subjects: APC antigen presenting cells -- CRD carbohydrate recognition domain -- DCs dendritic cells -- GDF-15 growth differentiation factor-15 -- IL interleukin -- IDO indoleamine 2, 3-dioxygenase -- IFN-γ interferon-γ -- LXR liver X receptors -- M-CSF macrophage-colony stimulating factor -- mAbs monoclonal antibodies -- NO nitric oxide -- NOS nitric oxide synthase -- RNS reactive nitrogen species -- ROS reactive oxygen species -- SULT2B1b sulfotransferase 2B1b -- TCR T cell receptor -- TGF-β transforming growth factor-β -- TILs tumor infiltrating lymphocytes -- Th T helper -- TNF-α tumor necrosis factor-α -- TSLP thymic stromal lymphopoietin -- VEGF vascular endothelial growth factor -- XBP1 x-box-binding protein 1; Tumor microenvironment -- Immunosuppressive factors -- Dendritic cells -- T cells; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2017.06.005
• Languages: English
• ISSNs: 1359-6101

Abstract

Abstract: Tumor progression is accompanied by the production of a wide array of immunosuppressive factors by tumor and non-tumor cells forming the tumor microenvironment. These factors belonging to cytokines, growth factors, metabolites, glycan-binding proteins and glycoproteins are responsible for the establishment of immunosuppressive networks leading towards tumor promotion, invasion and metastasis. In pre-clinical tumor models, the inactivation of some of these suppressive networks reprograms the phenotypic and functional features of tumor-infiltrating immune cells, ultimately favoring effective anti-tumor immune responses. We will discuss factors and mechanisms identified in both mouse and human tumors, and the possibility to associate drugs inhibiting these mechanisms with new immunotherapy strategies already entered in the clinical practice.