Caspase-independent cell death in T lymphocytes

Details

Serval ID
serval:BIB_6078FA3FEED8
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Caspase-independent cell death in T lymphocytes
Journal
Nature Immunology
Author(s)
Jaattela  M., Tschopp  J.
ISSN
1529-2908 (Print)
Publication state
Published
Issued date
05/2003
Volume
4
Number
5
Pages
416-23
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review --- Old month value: May
Abstract
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.
Keywords
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
Create date
24/01/2008 15:18
Last modification date
20/08/2019 14:17
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