|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 189, Number 3, February 1, 1999 575-586
By
From the * Division of Molecular Immunology and the 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.
Division of Cellular Immunology, MRC
National Institute for Medical Research, London NW7 1AA, United Kingdom; the § Division of
Molecular Genetics, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; and the Cancer Biology and Molecular Haematology Units, Camelia Botnar Laboratories, Institute of Child
Health, London WC1N 1EH, United Kingdom
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
