Tumor stress, cell death and the ensuing immune response.
A cornucopia of physiological and pathological circumstances including anticancer chemotherapy and radiotherapy can induce cell death. However, the immunological consequences of tumor cell demise have remained largely elusive. The paradigm opposing 'apoptosis versus necrosis' as to their respective immunogenicity does not currently hold to predict long-term immunity. Moreover, the notion that tumor cells may be 'stressed' before death to be recognized by immune cells deserves to be underlined. 'Eat-me', 'danger' and 'killing' signals released by stressed tumor under the pressure of cytotoxic compounds may serve as links between the chemotherapy-elicited response of tumor cells and subsequent immune responses. This review will summarize the state-of-the-art of cancer immunity and describe how tumor cell death dictates the links between innate and acquired immunity.
Ullrich
E
E
INSERM U805, Institut Gustave Roussy, Pavillon de Recherche 1, 39 rue Camille Desmoulins, Villejuif, France.
Bonmort
M
M
Mignot
G
G
Kroemer
G
G
Zitvogel
L
L
D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D016923:Cell Death; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D003713:Dendritic Cells / Q000276:immunology; D006801:Humans; D007110:Immunity, Active; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology; D008954:Models, Biological; D009336:Necrosis; D009369:Neoplasms / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology*; D015398:Signal Transduction; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
D016207:Cytokines