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bcl-2 inhibits multiple forms of apoptosis but not negative selection in thymocytes.

The vast majority of cortical thymocytes die during T cell development while those that survive this selective process accumulate in the medulla. bcl-2, an inner mitochondrial membrane protein, has been shown to inhibit apoptosis in certain cell lines. In the thymus, bcl-2 is regionally localized to the mature T cells of the medulla. To assess the role of bcl-2 in the programmed death of thymocytes, we generated transgenic mice that redirected bcl-2 expression to cortical thymocytes. bcl-2 protected immature CD4+8+ thymocytes from glucocorticoid, radiation, and anti-CD3-induced apoptosis. Moreover, bcl-2 altered T cell maturation, resulting in increased percentages of CD3hi and CD4-8+ thymocytes. Despite this, clonal deletion of T cells that recognize endogenous superantigens still occurred. This transgenic model indicates that multiple death pathways operate within the thymus that can be distinguished by their dependence on bcl-2.

Pubmed ID: 1835668


  • Sentman CL
  • Shutter JR
  • Hockenbery D
  • Kanagawa O
  • Korsmeyer SJ



Publication Data

November 29, 1991

Associated Grants

  • Agency: NCI NIH HHS, Id: P01 CA49712-03

Mesh Terms

  • Animals
  • Antigens, CD3
  • Antigens, CD4
  • Antigens, CD8
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Surface
  • Blotting, Western
  • Cell Death
  • Cell Survival
  • Dexamethasone
  • Flow Cytometry
  • Growth Hormone
  • Humans
  • Kinetics
  • Lymph Nodes
  • Mice
  • Mice, Inbred Strains
  • Mice, Transgenic
  • Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogenes
  • Receptors, Antigen, T-Cell
  • Restriction Mapping
  • T-Lymphocyte Subsets
  • T-Lymphocytes