Home LiteratureArticle Details
PMID: 8326141 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

bcl-2 proto-oncogene expression during human T cell development. Evidence for biphasic regulation.

Journal of immunology (Baltimore, Md. : 1950) ·Vol. 151 ·No. 1 ·1993-07-01 ·Pages 83-91

Gratiot-Deans J, Ding L, Turka LA, Nuñez G

Abstract

To ensure that the mature T cell repertoire is MHC-restricted yet not autoreactive, cortical thymocytes that express low levels of the TCR/CD3 complex along with CD4 and CD8 (double positive cells) are subjected to positive and negative selection. Surviving cells lose either CD4 or CD8 (single positive cells) and are located primarily in the thymic medulla. bcl-2, a novel proto-oncogene that promotes cell survival by inhibiting programmed cell death (apoptosis), may be an important protein in regulating cell survival during thymocyte development. We have examined the expression of bcl-2 during T cell development by using human thymocytes. Consistent with previous studies, human thymic tissue sections stained for bcl-2 revealed occasional bcl-2+ cells within the thymic cortex and intense staining of virtually all medullary thymocytes. More quantitative western blot analysis and S1 nuclease protection assay revealed that single positive thymocytes contained approximately 2 to 3 times the level of bcl-2 protein and 3 to 4 times the level of bcl-2 mRNA as double positive thymocytes. Flow cytometric analysis of purified double positive thymocytes revealed that minimal amounts of bcl-2 protein was in fact detectable in most cells, although a small subpopulation (10-20%) contained higher levels. In contrast, brighter staining for bcl-2 was observed in virtually all single positive thymocytes. Surprisingly, CD4-CD8- thymocytes (both CD3- and CD3+) expressed the same amount of bcl-2 as did the single positive thymocytes. Because a large percentage of CD3-CD4-CD8- cells are cycling, we examined the effect of mitogenic stimulation on bcl-2 expression by double positive thymocytes by using western blot analysis. bcl-2 expression in double positive thymocytes could not be induced by cell cycle entry following stimulation with PMA and ionomycin. Our data demonstrate that bcl-2 expression is biphasic during T cell development. Both CD3-CD4-CD8- and CD3+CD4+ and CD3+CD8+ thymocytes express high levels of bcl-2. Therefore, diminished bcl-2 expression in double positive thymocytes seems to be the result of specific down-regulation in order to facilitate the selection CD4+CD8+ thymocytes.

Related Genes
MeSH Terms
Cell Differentiation Child, Preschool Flow Cytometry Gene Expression Humans Infant Ionomycin/pharmacology Proto-Oncogene Mas Proto-Oncogene Proteins/genetics Proto-Oncogene Proteins c-bcl-2 Proto-Oncogenes RNA, Messenger/genetics T-Lymphocyte Subsets/cytology,metabolism T-Lymphocytes/cytology,metabolism Tetradecanoylphorbol Acetate/pharmacology Thymus Gland/cytology
Chemicals
MAS1 protein, human Proto-Oncogene Mas Proto-Oncogene Proteins Proto-Oncogene Proteins c-bcl-2 RNA, Messenger Ionomycin Tetradecanoylphorbol Acetate
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Gratiot-Deans J
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109.
Ding L
Turka L A
Nuñez G
Article Info
Journal
Journal of immunology (Baltimore, Md. : 1950)
Abbr.
J Immunol
ISSN
0022-1767
Published
1993-07-01
Pages
83-91
Language
English
Region
United States
NLM ID
2985117R
Subset
IM
Grants
NIDDK NIH HHS · DK01899 · United States
NIDDK NIH HHS · DK44737 · United States
NIAMS NIH HHS · UM-MAC-P60-AR20557 · United States
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]