Abstract
Activated T cells use apoptosis as a regulatory mechanism to prevent an exaggerated immune response. Repetitive or sustained stimulation of the T-cell receptor (TCR) induces surface expression of Fas and its ligand (FasL). Binding of FasL to its receptor initiates a signaling pathway resulting in the death of Fas-expressing T cells. Defects in Fas-mediated apoptosis cause autoimmune lymphoproliferative syndrome (ALPS), which is characterized by lymphoproliferation, autoimmune cytopenia, susceptibility to lymphoma, and accumulation of TCRαβ+CD4–CD8– (double-negative) T cells.
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