Bad can act as a key regulator of T cell apoptosis and T cell development
File(s)
Author(s)
Type
Journal Article
Abstract
Bad is a distant relative of Bcl-2 and acts to promote cell death. Here, we show that Bad expression levels are greatly increased in thymocytes during apoptosis. We generated bad transgenic mice to study the action of upregulated Bad expression on T cell apoptosis. The T cells from these mice are highly sensitive to apoptotic stimuli, including anti-CD95. The numbers of T cells are greatly depleted and the processes of T cell development and selection are perturbed. We show that the proapoptotic function of Bad in primary T cells is regulated by Akt kinase and that Bad overexpression enhances both cell cycle progression and interleukin 2 production after T cell activation. These data suggest that Bad can act as a key regulator of T cell apoptosis and that this is a consequence of its upregulation after exposure to death stimuli.
Date Issued
1999-02-01
Date Acceptance
1998-09-01
Citation
Journal of Experimental Medicine, 1999, 189 (3), pp.575-586
ISSN
0022-1007
Publisher
Rockefeller University Press
Start Page
575
End Page
586
Journal / Book Title
Journal of Experimental Medicine
Volume
189
Issue
3
Copyright Statement
© The Rockefeller University Press
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000078470300014&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Subjects
Science & Technology
Life Sciences & Biomedicine
Immunology
Medicine, Research & Experimental
Research & Experimental Medicine
Bad
apoptosis
selection
cell cycle
Akt
RECEPTOR TRANSGENIC MICE
PROTEIN-KINASE
NEGATIVE SELECTION
PHOSPHATIDYLINOSITOL 3-KINASE
MONOCLONAL-ANTIBODIES
BCL-2 TRANSGENE
CYCLE ENTRY
GENE FAMILY
BH3 DOMAIN
B-CELLS
Publication Status
Published
Date Publish Online
1998-09-16