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| Activation-induced cell death (AICD) ： ウィキペディア英語版 |
Activation-induced cell death (AICD)
AICD (activation-induced cell death) is programmed cell death caused by the interaction of Fas receptors (Fas, CD95) and Fas ligands (FasL, CD95 ligand).〔Zhang J, Xu X, Liu Y. (2004), Activation-Induced Cell Death in T Cells and Autoimmunity. Cell Mol Immunol. 1(3):186-92〕 AICD is a negative regulator of activated T lymphocytes that results from repeated stimulation of their T-cell receptors (TCR) and helps to maintain peripheral immune tolerance.〔Kabelitz D, Janssen O. (1997), Antigen-induced death of T-lymphocytes. Front Biosci. 2:d61-77〕 Alteration of the process may lead to autoimmune diseases.〔
The AICD effector cell is one that expresses FasL, and apoptosis is induced in the cell expressing the Fas receptor. Both activated T cells and B cells express Fas and undergo clonal deletion by the AICD mechanism.〔Green DR, Droin N, Pinkoski M. (2003), Activation-induced cell death in T cells. Immunol Rev. 193:70-81〕〔Donjerković D, Scott DW. (2000), Activation-induced cell death in B lymphocytes. Cell Res. 10(3):179-92〕 Activated T cells that express both Fas and FasL may be killed by themselves or by each other.〔
== Signaling ==
The binding of Fas ligand to Fas triggers trimerization of Fas, whose cytoplasmic domain is then able to bind the death domain of the adaptor protein FADD (Fas-associated protein with death domain). Procaspase 8 binds to FADD's death effector domain (DED) and proteolytically self-activates as caspase 8. Fas, FADD, and procaspase 8 together form a death-inducing signaling complex (DISC). Activated caspase 8 is released into the cytosol, where it activates the caspase cascade that initiates apoptosis.〔Nagata S. (1997), Apoptosis by death factor. Cell. 88(3):355-65〕〔
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