Caspase-independent cell death in T lymphocytes
Détails
ID Serval
serval:BIB_6078FA3FEED8
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Caspase-independent cell death in T lymphocytes
Périodique
Nature Immunology
ISSN
1529-2908 (Print)
Statut éditorial
Publié
Date de publication
05/2003
Volume
4
Numéro
5
Pages
416-23
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review --- Old month value: May
Research Support, Non-U.S. Gov't
Review --- Old month value: May
Résumé
T lymphocyte death is essential for proper function of the immune system. During the decline of an immune response, most of the activated T cells die. Cell death is also responsible for eliminating autoreactive lymphocytes. Although recent studies have focused on caspase-dependent apoptotic signals, much evidence now shows that caspase- independent, necrotic cell death pathways are as important. An understanding of the molecular control of these alternative pathways is beginning to emerge. Damage of organelles including mitochondria, endoplasmic reticulum or lysozymes, leading to an increase in calcium and reactive oxygen species and the release of effector proteins, is frequently involved in caspase-independent cell death.
Mots-clé
Animals
Antigens, CD/physiology
Antigens, CD95/physiology
Apoptosis/physiology
Calcium Signaling
Caspases/*metabolism
Cell Death/*physiology
Endoplasmic Reticulum/physiology
Humans
Lysosomes/physiology
Mice
Mitochondria/physiology
Models, Biological
Receptors, Tumor Necrosis Factor/physiology
Receptors, Tumor Necrosis Factor, Type I
T-Lymphocytes/*cytology/*enzymology/immunology
Pubmed
Web of science
Création de la notice
24/01/2008 16:18
Dernière modification de la notice
20/08/2019 15:17