FAS AND FASL IN THE HOMEOSTATIC REGULATION OF IMMUNE-RESPONSES
被引:530
作者:
LYNCH, DH
论文数: 0引用数: 0
h-index: 0
机构:DARWIN MOLEC, BOTHELL, WA 98021 USA
LYNCH, DH
RAMSDELL, F
论文数: 0引用数: 0
h-index: 0
机构:DARWIN MOLEC, BOTHELL, WA 98021 USA
RAMSDELL, F
ALDERSON, MR
论文数: 0引用数: 0
h-index: 0
机构:DARWIN MOLEC, BOTHELL, WA 98021 USA
ALDERSON, MR
机构:
[1] DARWIN MOLEC, BOTHELL, WA 98021 USA
[2] CORIAX CORP, SEATTLE, WA 98104 USA
来源:
IMMUNOLOGY TODAY
|
1995年
/
16卷
/
12期
关键词:
D O I:
10.1016/0167-5699(95)80079-4
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Studies of the biological effects of Fas signaling, using transformed cell lines as targets, indicate that ligation of the Fas receptor induces an apoptotic death signal. Chronically activated normal human T cells are also susceptible to Fas-mediated apoptosis. However, interactions between Fas and Fas ligand can also yield a costimulatory signal. Here, David Lynch, Fred Ramsdell and Mark Alderson present a model for the role of Fas and Fast in the homeostatic regulation of normal immune responses. They discuss how dysregulation of the Fas apoptotic pathway may contribute to certain disease states, including autoimmune disease and human immunodeficiency virus (HIV)-induced depletion of CD4(+) T cells.