4.8 Article

Caspases Connect Cell-Death Signaling to Organismal Homeostasis

Journal

IMMUNITY
Volume 44, Issue 2, Pages 221-231

Publisher

CELL PRESS
DOI: 10.1016/j.immuni.2016.01.020

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Funding

  1. Ligue contre le Cancer (equipe labellisee)
  2. Agence National de la Recherche (ANR) - Projets blancs
  3. ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases
  4. Association pour la Recherche sur le Cancer (ARC)
  5. Canceropole Ile-de-France
  6. Institut National du Cancer (INCa)
  7. Fondation Bettencourt-Schueller
  8. Fondation de France
  9. Fondation pour la Recherche Medicale (FRM)
  10. European Commission (ArtForce)
  11. European Research Council (ERC)
  12. LabEx Immuno-Oncology
  13. SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
  14. SIRIC Cancer Research and Personalized Medicine (CARPEM)
  15. Paris Alliance of Cancer Research Institutes (PACRI)
  16. National Health and Medical Research Council (NHMRC) of Australia

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Some forms of regulated cell death, such as apoptosis, are precipitated by the activation of cysteine proteases of the caspase family, including caspase 8, 9, and 3. Other caspases, such as caspase 1 and 4, are well known for their pro-inflammatory functions but regulate cell death in a limited number of pathophysiological settings. Accumulating evidence suggests that the most conserved function of mammalian caspases is not to control cell death sensu stricto, but to regulate inflammatory and immune reactions to dying cells and infectious challenges. Here, we review the molecular and cellular mechanisms though which mammalian caspases connect cell-death signaling to the maintenance of organismal homeostasis.

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