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The regulation of FasL expression during activation‐induced cell death (AICD)
Author(s) -
Nguyen Thang,
Russell John
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01264.x
Subject(s) - fas ligand , endocytosis , microbiology and biotechnology , jurkat cells , biology , apoptosis , programmed cell death , chemistry , t cell , cell , immunology , immune system , biochemistry
Summary Activation‐induced cell death (AICD), a Fas ligand (FasL)‐dependent pathway, is important for maintaining T‐cell homeostasis. Interleukin‐2 (IL‐2), an enhancer of AICD, can also enhance FasL expression. However, we show that the level of FasL or FLIP protein did not correlate with the susceptibility to AICD. Some T cells expressed high levels of FasL yet failed to undergo AICD, while others expressed little FasL and were sensitive. AICD susceptibility did not correlate with the kinetics of FasL up‐regulation or down‐regulation. The down‐regulation of FasL can be mediated by a metalloprotease. However, we describe an alternative mechanism for the loss of FasL by endocytosis. Endocytosis inhibitors such as cytochalasins, sodium azide, deoxyglucose, or low temperatures prevented the loss of FasL. KB8301, a metalloprotease inhibitor had no effect on the loss of FasL or AICD in the T cells. Enhancing FasL expression was not crucial for AICD and the down‐regulation of FasL proceeded via endocytosis.