Journal
ANNUAL REVIEW OF IMMUNOLOGY, VOL 31
Volume 31, Issue -, Pages 51-72Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-032712-100008
Keywords
ATP; autophagy; calreticulin; damage-associated molecular patterns; HMGB1; TLR4
Categories
Funding
- Ligue Nationale contre le Cancer (Equipe Labellisee)
- Agence Nationale pour la Recherche (ANR)
- European Commission (Active p53, Apo-Sys, ChemoRes, ApopTrain)
- Institut National du Cancer (INCa)
- Canceropole Ile-de-France
- Fondation Bettencourt-Schueller
- AXA Research Fund
- LabEx Immuno-Oncology
- Paris Alliance of Cancer Research Institutes
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Depending on the initiating stimulus, cancer cell death can be immunogenic or nonimmunogenic. Immunogenic cell death (ICD) involves changes in the composition of the cell surface as well as the release of soluble mediators, occurring in a defined temporal sequence. Such signals operate on a series of receptors expressed by dendritic cells to stimulate the presentation of tumor antigens to T cells. We postulate that ICD constitutes a prominent pathway for the activation of the immune system against cancer, which in turn determines the long-term success of anticancer therapies. Hence, suboptimal regimens (failing to induce ICD), selective alterations in cancer cells (preventing the emission of immunogenic signals during ICD), or defects in immune effectors (abolishing the perception of ICD by the immune system) can all contribute to therapeutic failure. We surmise that ICD and its subversion by pathogens also play major roles in antiviral immune responses.
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