TY - JOUR
T1 - Activation-induced cell death in T cells
AU - Green, Douglas R.
AU - Droin, Nathalie
AU - Pinkoski, Michael
PY - 2003/6/1
Y1 - 2003/6/1
N2 - A properly functioning immune system is dependent on programmed cell death at virtually every stage of lymphocyte development and activity. This review addresses the phenomenon of activation-induced cell death (AICD) in T lymphocytes, in which activation through the T-cell receptor results in apoptosis. AICD can occur in a cell-autonomous manner and is influenced by the nature of the initial T-cell activation events. It plays essential roles in both central and peripheral deletion events involved in tolerance and homeostasis, although it is likely that different forms of AICD proceed via different mechanisms. For example, while AICD in peripheral T cells is often caused by the induction of expression of the death ligand, Fas ligand (CD95 ligand, FasL), it does not appear to be involved in AICD in thymocytes. This and other mechanisms of AICD are discussed. One emerging model that may complement other forms of AICD involves the inducible expression of FasL by nonlymphoid tissues in response to activated T lymphocytes. Induction of nonlymphoid FasL in this manner may serve as a sensing mechanism for immune cell infiltration, which contributes to peripheral deletion.
AB - A properly functioning immune system is dependent on programmed cell death at virtually every stage of lymphocyte development and activity. This review addresses the phenomenon of activation-induced cell death (AICD) in T lymphocytes, in which activation through the T-cell receptor results in apoptosis. AICD can occur in a cell-autonomous manner and is influenced by the nature of the initial T-cell activation events. It plays essential roles in both central and peripheral deletion events involved in tolerance and homeostasis, although it is likely that different forms of AICD proceed via different mechanisms. For example, while AICD in peripheral T cells is often caused by the induction of expression of the death ligand, Fas ligand (CD95 ligand, FasL), it does not appear to be involved in AICD in thymocytes. This and other mechanisms of AICD are discussed. One emerging model that may complement other forms of AICD involves the inducible expression of FasL by nonlymphoid tissues in response to activated T lymphocytes. Induction of nonlymphoid FasL in this manner may serve as a sensing mechanism for immune cell infiltration, which contributes to peripheral deletion.
UR - http://www.scopus.com/inward/record.url?scp=0038171458&partnerID=8YFLogxK
U2 - 10.1034/j.1600-065X.2003.00051.x
DO - 10.1034/j.1600-065X.2003.00051.x
M3 - Review article
C2 - 12752672
AN - SCOPUS:0038171458
SN - 0105-2896
VL - 193
SP - 70
EP - 81
JO - Immunological Reviews
JF - Immunological Reviews
ER -