Abstract
The bclx gene has been shown to regulate programmed cell death in vitro. We now show that Bclx expression increases dramatically when T cells differentiate from CD4- CD8- (double negative) thymocytes to CD4+ CD8+ [double positive (DP)] thymocytes. In contrast single-positive (SP) thymocytes express negligible amounts of Bclx protein. This expression pattern contrasts with that of Bcl2, which is present in double-negative thymocytes, down-regulated in DP thymocytes, and reinduced upon maturation to SP thymocytes. Elimination of Bclx by gene targeting dramatically shortens the survival of DP thymocytes but not the survival of SP thymocytes or peripheral SP T cells. These data suggest that the induction of Bclx during thymic maturation plays a critical role in regulating the length of time DP thymocytes survive in the absence of selection.
MeSH Terms
Animals
Antibodies, Monoclonal
CD4 Antigens/analysis
CD8 Antigens/analysis
Cell Death
Cell Survival/immunology
Cells, Cultured
Embryo, Mammalian
Gene Expression
Mice/immunology
Proto-Oncogene Proteins/biosynthesis
Proto-Oncogene Proteins c-bcl-2
Recombinant Proteins/biosynthesis,immunology
Stem Cells/immunology
T-Lymphocyte Subsets/cytology,immunology
T-Lymphocytes/cytology,immunology
bcl-X Protein
Chemicals
Antibodies, Monoclonal
Bcl2l1 protein, mouse
CD4 Antigens
CD8 Antigens
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-bcl-2
Recombinant Proteins
bcl-X Protein
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Ma A
Howard Hughes Medical Institute, Children's Hospital, Boston, MA, USA.
Pena J C
Chang B
Margosian E
Davidson L
Alt F W
Thompson C B
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