Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (14)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Tomayko, M. M.
Right arrow Articles by Cancro, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tomayko, M. M.
Right arrow Articles by Cancro, M. P.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 11, No. 11, 1753-1761, November 1999
© 1999 Japanese Society for Immunology

Expression of the Bcl-2 family member A1 is developmentally regulated in T cells

Mary M. Tomayko, Jennifer A. Punt1, Jeffrey M. Bolcavage1, Sherri L. Levy, David M. Allman2 and Michael P. Cancro

Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6082, USA
1 Department of Biology, Haverford College, Haverford, PA 19041, USA
2 Fox Chase Cancer Center, Philadelphia, PA 19111, USA

Correspondence to: M. P. Cancro

During T cell development, cells that fail to meet stringent selection criteria undergo programmed cell death. Thymocyte and peripheral T cell susceptibility to apoptosis is influenced by expression of Bcl-2 family members, some of which are expressed in a developmentally patterned manner. We previously showed developmentally regulated expression of A1, an anti-apoptotic Bcl-2 family member, among B cell developmental subsets. Here we show that cells of the T lineage also express A1 in a developmentally regulated manner. Both A1 mRNA and A1 protein are readily detectable in the thymus, and while present among DN cells, A1 mRNA is up-regulated to very high levels among double-positive (DP) thymocytes. It is then down-regulated to moderate levels among single-positive (SP) thymocytes, and finally expressed at ~25-fold lower levels among mature SP CD4+ and CD8+ lymph node T cells than among DP thymocytes. Furthermore, we find that in vitro TCR ligation up-regulates A1 expression among both DP and SP thymocytes. Together, these data show that A1 expression is developmentally regulated in T lymphocytes and is responsive to TCR signaling, suggesting that A1 may play a role in maintaining the viability of DP thymocytes.

Keywords: apoptosis, FACS, gene regulation, maturation, molecular biology, mouse, T lymphocytes

Transmitting editor: A. Singer


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Immunol.Home page
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]


Home page
J. Immunol.Home page
D. DeRyckere, D. L. Mann, and J. DeGregori
Characterization of Transcriptional Regulation During Negative Selection In Vivo
J. Immunol., July 15, 2003; 171(2): 802 - 811.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
J. Gonzalez, A. Orlofsky, and M. B. Prystowsky
A1 is a growth-permissive antiapoptotic factor mediating postactivation survival in T cells
Blood, April 1, 2003; 101(7): 2679 - 2685.
[Abstract] [Full Text] [PDF]


Home page
BloodHome page
P. I. Chuang, S. Morefield, C.-Y. Liu, S. Chen, J. M. Harlan, and D. M. Willerford
Perturbation of B-cell development in mice overexpressing the Bcl-2 homolog A1
Blood, May 1, 2002; 99(9): 3350 - 3359.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.