4.6 Review Book Chapter

Immunogenic Cell Death in Cancer Therapy

期刊

ANNUAL REVIEW OF IMMUNOLOGY, VOL 31
卷 31, 期 -, 页码 51-72

出版社

ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-032712-100008

关键词

ATP; autophagy; calreticulin; damage-associated molecular patterns; HMGB1; TLR4

资金

  1. Ligue Nationale contre le Cancer (Equipe Labellisee)
  2. Agence Nationale pour la Recherche (ANR)
  3. European Commission (Active p53, Apo-Sys, ChemoRes, ApopTrain)
  4. Institut National du Cancer (INCa)
  5. Canceropole Ile-de-France
  6. Fondation Bettencourt-Schueller
  7. AXA Research Fund
  8. LabEx Immuno-Oncology
  9. Paris Alliance of Cancer Research Institutes

向作者/读者索取更多资源

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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