title: Activation-induced cell death.
abstract: The death of T lymphocytes following their activation involves several signal pathways that converge on a series of proteases, known as caspases, that degrade cellular proteins and activate a DNAse. Caspases are activated through ligation of cell surface death receptors as well as via direct activation of downstream caspases, often through metabolic stress such as cytokine withdrawal or generation of oxygen radicals, that culminates in mitochondrial dysfunction and release of the pro-apoptotic molecules, cytochrome c and Smac/DIABLO. The Bcl-2 family members serve to regulate the mitochondrial membrane integrity. Recent studies are now revealing the significant contribution to the activation-induced cell death of T cells by downstream caspases such as caspase-3 and Bcl-2-homology domain 3 (BH3)-only members of the Bcl-2 family.
authors.affiliation: Immunobiology Program, The University of Vermont College of Medicine, Given Medical Building, D-305 05405-0068, Burlington, VT, USA. rbodd@zoo.uvm.edu
authors.forename: R C
authors.initials: RC
authors.lastname: Budd
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000502:physiology*; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D015398:Signal Transduction / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology / Q000201:enzymology / Q000276:immunology / Q000378:metabolism; D019014:fas Receptor / Q000502:physiology
chemical_list: D018124:Receptors, Tumor Necrosis Factor; D019014:fas Receptor