|
|
Prepublished online as a Blood First Edition Paper on October 24, 2002; DOI 10.1182/blood-2002-04-1229.
 Previous Article | Table of Contents | Next Article 
Blood, 1 April 2003, Vol. 101, No. 7, pp. 2679-2685
IMMUNOBIOLOGY
A1 is a growth-permissive antiapoptotic factor mediating
postactivation survival in T cells
Juana Gonzalez,
Amos Orlofsky, and
Michael B. Prystowsky
From the Department of Pathology, Albert Einstein
College of Medicine, Bronx, NY.
The regulation of cell death in activated naive T cells is not well
understood. We examined the expression of A1, an antiapoptotic member
of the Bcl-2 family, following activation of naive mouse splenocytes.
A1 gene expression was strongly but transiently induced during the
first day of activation, with a peak at 2 to 6 hours, whereas Bcl-2
mRNA was simultaneously transiently down-regulated. Transgenic (Tg) overexpression of A1-a in T cells via the lck distal promoter resulted in decreased apoptosis following activation either with concanavalin A or with antibodies to CD3 and CD28 and led
to a doubling of T-cell yield by 5 days. Tg A1-a also partially
protected thymocytes from several proapoptotic stimuli but did not
protect T-cell blasts from cell death induced by reactivation via the
T-cell receptor. Tg Bcl-2 and Tg A1-a showed a similar ability
to reduce apoptosis in both resting and activated T cells. However, in
activated splenocyte cultures, the increase in 5-day T-cell yield
observed with Tg Bcl-2 was only half that produced by Tg A1-a. This
difference could be attributed at least in part to the fact that A1,
unlike Bcl-2, did not inhibit S-phase entry of activated cells. The A1
protein may represent an adaptation of the Bcl-2 gene family to the
need for survival regulation in the context of a proliferative stimulus.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
J. Gonzalez, E. Tamayo, I. Santiuste, R. Marquina, L. Buelta, M. A. Gonzalez-Gay, S. Izui, M. Lopez-Hoyos, J. Merino, and R. Merino
CD4+CD25+ T Cell-Dependent Inhibition of Autoimmunity in Transgenic Mice Overexpressing Human Bcl-2 in T Lymphocytes
J. Immunol.,
March 1, 2007;
178(5):
2778 - 2786.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. J. Herold, J. Zeitz, C. Pelzer, C. Kraus, A. Peters, G. Wohlleben, and I. Berberich
The Stability and Anti-apoptotic Function of A1 Are Controlled by Its C Terminus
J. Biol. Chem.,
May 12, 2006;
281(19):
13663 - 13671.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Rasooly, G. U. Schuster, J. P. Gregg, J.-H. Xiao, R. A. S. Chandraratna, and C. B. Stephensen
Retinoid X Receptor Agonists Increase Bcl2a1 Expression and Decrease Apoptosis of Naive T Lymphocytes
J. Immunol.,
December 15, 2005;
175(12):
7916 - 7929.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Oberdoerffer, C. Kanellopoulou, V. Heissmeyer, C. Paeper, C. Borowski, I. Aifantis, A. Rao, and K. Rajewsky
Efficiency of RNA Interference in the Mouse Hematopoietic System Varies between Cell Types and Developmental Stages
Mol. Cell. Biol.,
May 15, 2005;
25(10):
3896 - 3905.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Mandal, C. Borowski, T. Palomero, A. A. Ferrando, P. Oberdoerffer, F. Meng, A. Ruiz-Vela, M. Ciofani, J.-C. Zuniga-Pflucker, I. Screpanti, et al.
The BCL2A1 gene as a pre-T cell receptor-induced regulator of thymocyte survival
J. Exp. Med.,
February 22, 2005;
201(4):
603 - 614.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
I. Schmitz, L. K. Clayton, and E. L. Reinherz
Gene expression analysis of thymocyte selection in vivo
Int. Immunol.,
October 1, 2003;
15(10):
1237 - 1248.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
