Caspase-independent cell death in T lymphocytes.
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.
Apoptosis Laboratory, Institute of Cancer Biology, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. mhj@biobase.dk
Marja
M
Jäättelä
Jürg
J
Tschopp
D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D017209:Apoptosis / Q000502:physiology; D020013:Calcium Signaling; D020169:Caspases / Q000378:metabolism*; D016923:Cell Death / Q000502:physiology*; D004721:Endoplasmic Reticulum / Q000502:physiology; D006801:Humans; D008247:Lysosomes / Q000502:physiology; D051379:Mice; D008928:Mitochondria / Q000502:physiology; D008954:Models, Biological; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D047888:Receptors, Tumor Necrosis Factor, Type I; D013601:T-Lymphocytes / Q000166:cytology* / Q000201:enzymology* / Q000276:immunology; D019014:fas Receptor / Q000502:physiology
D015703:Antigens, CD; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D019014:fas Receptor; D020169:Caspases