title: [Breaking immune tolerance in cancer].
abstract: The discovery and understanding of complex cellular interactions that govern the immune system contributed to the pharmacological targeting of anti-tumor immunity. The activity of immune effector cells, such as NK and T-cells, is regulated by a wide range of activating and inhibiting receptors or ligands. Drugs that target these receptors or ligands can modulate the immune response by exerting antagonistic or agonistic effects. Over the past decade, several immunomodulators have demonstrated clinical effectiveness, and three of them have already been approved for use in oncology. The development of these immunotherapy approaches presented unique challenges for safety and efficacy, requiring revising clinical response criteria and the establishment of guidelines to help oncologists to manage properly inflammatory toxicities. The introduction of these immunotherapies is a revolution in oncology. However, additional efforts in terms of optimizing treatment administration and identification of biomarkers are needed. Identifying the immunodynamics of various immunomodulators should allow a better understanding of anti-tumor and inflammatory mechanisms, and certainly give the opportunity to develop effective therapeutic combinations without potentiating adverse events.
authors.affiliation: Gustave-Roussy cancer campus, 39, rue Camille-Desmoulins, 94805 Villejuif, France; Gustave-Roussy cancer campus, centre d'investigation clinique biothérapie 1428, Inserm, 39, rue Camille-Desmoulins, 94805 Villejuif, France; Université Paris-Sud, faculté de médecine, 63, rue Gabriel-Péri, 94270 Kremlin-Bicêtre, France; Gustave-Roussy cancer campus, laboratoire d'immunomonitoring en oncologie, UMS 3655 CNRS et US 23 Inserm, 39, rue Camille-Desmoulins, 94805 Villejuif, France.
authors.forename: Mélanie
authors.initials: M
authors.lastname: Desbois
authors.affiliation: Gustave-Roussy cancer campus, 39, rue Camille-Desmoulins, 94805 Villejuif, France; Gustave-Roussy cancer campus, département des innovations thérapeutiques et d'essais précoces (DITEP), 39, rue Camille-Desmoulins, 94805 Villejuif, France; Institut de cancérologie de l'Ouest, boulevard Jacques-Monod, 44800 Saint-Herblain, France.
authors.forename: Stéphane
authors.initials: S
authors.lastname: Champiat
authors.affiliation: Gustave-Roussy cancer campus, 39, rue Camille-Desmoulins, 94805 Villejuif, France; Gustave-Roussy cancer campus, centre d'investigation clinique biothérapie 1428, Inserm, 39, rue Camille-Desmoulins, 94805 Villejuif, France; Gustave-Roussy cancer campus, laboratoire d'immunomonitoring en oncologie, UMS 3655 CNRS et US 23 Inserm, 39, rue Camille-Desmoulins, 94805 Villejuif, France. Electronic address: CHAPUT-GRAS.Nathalie@gustaveroussy.fr.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Chaput
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D000951:Antigens, Neoplasm / Q000276:immunology; D060908:CTLA-4 Antigen / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D007155:Immunologic Factors / Q000627:therapeutic use*; D007167:Immunotherapy; D007211:Indoles / Q000627:therapeutic use; D000074324:Ipilimumab; D007694:Killer Cells, Natural / Q000502:physiology; D008545:Melanoma / Q000276:immunology / Q000628:therapy; D009369:Neoplasms / Q000276:immunology* / Q000628:therapy*; D000077594:Nivolumab; D013449:Sulfonamides / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000502:physiology; D059016:Tumor Microenvironment / Q000276:immunology; D000077484:Vemurafenib
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000951:Antigens, Neoplasm; D060908:CTLA-4 Antigen; D007155:Immunologic Factors; D007211:Indoles; D000074324:Ipilimumab; D013449:Sulfonamides; D000077484:Vemurafenib; D000077594:Nivolumab; C585832:pidilizumab; C582435:pembrolizumab; C520704:tremelimumab
keywords: CTLA-4; Cancer; Immune checkpoints; Immunity; Immunité; Microenvironnement tumoral; PD-1; PD-L1; Tumor microenvironment