title: Immunogenic Apoptotic Cell Death and Anticancer Immunity.
abstract: For many years it has been thought that apoptotic cells rapidly cleared by phagocytic cells do not trigger an immune response but rather have anti-inflammatory properties. However, accumulating experimental data indicate that certain anticancer therapies can induce an immunogenic form of apoptosis associated with the emission of damage-associated molecular patterns (DAMPs), which function as adjuvants to activate host antitumor immune responses. In this review, we will first discuss recent advances and the significance of danger signaling pathways involved in the emission of DAMPs, including calreticulin, ATP, and HMGB1. We will also emphasize that switching on a particular signaling pathway depends on the immunogenic cell death stimulus. Further, we address the role of ER stress in danger signaling and the classification of immunogenic cell death inducers in relation to how ER stress is triggered. In the final part, we discuss the role of radiotherapy-induced immunogenic apoptosis and the relationship of its immunogenicity to the fraction dose and concomitant chemotherapy.
authors: Molecular Signalling and Cell Death Unit, Inflammation Research Center, VIB, Ghent, Belgium.|Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.|Methusalem program, Ghent University, Ghent, Belgium.
authors: Peter
authors: P
authors: Vandenabeele
authors: Department of Radiation Oncology and Experimental Cancer Research, Ghent University, Ghent, Belgium.
authors: Katrien
authors: K
authors: Vandecasteele
authors: The Upper Airway Research Laboratory, Department of Oto-Rhino-Laryngology, Ghent University Hospital, Ghent, Belgium.
authors: Claus
authors: C
authors: Bachert
authors: The Upper Airway Research Laboratory, Department of Oto-Rhino-Laryngology, Ghent University Hospital, Ghent, Belgium.
authors: Olga
authors: O
authors: Krysko
authors: Molecular Signalling and Cell Death Unit, Inflammation Research Center, VIB, Ghent, Belgium. dmitri.krysko@ugent.be.|Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. dmitri.krysko@ugent.be.
authors: Dmitri V
authors: DV
authors: Krysko
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology; D000067531:Alarmins / Q000502:physiology; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology* / Q000528:radiation effects; D037282:Calreticulin / Q000502:physiology; D059248:Chemoradiotherapy; D019583:Dose Fractionation, Radiation; D059865:Endoplasmic Reticulum Stress / Q000502:physiology; D024243:HMGB1 Protein / Q000502:physiology; D006801:Humans; D051379:Mice; D009363:Neoplasm Proteins / Q000502:physiology; D009369:Neoplasms / Q000188:drug therapy / Q000276:immunology* / Q000532:radiotherapy; D017382:Reactive Oxygen Species; D015398:Signal Transduction / Q000502:physiology
chemical_list: D000067531:Alarmins; D000970:Antineoplastic Agents; D037282:Calreticulin; D024243:HMGB1 Protein; D009363:Neoplasm Proteins; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate
keywords: ATP; Calreticulin; Cancer; Chemotherapeutics; DAMPs; ER stress; HMGB1; Radiotherapy; Tumors