Enforced expression of Spi-B reverses T lineage commitment and blocks beta-selection

J Immunol. 2005 May 15;174(10):6184-94. doi: 10.4049/jimmunol.174.10.6184.

Abstract

The molecular changes that restrict multipotent murine thymocytes to the T cell lineage and render them responsive to Ag receptor signals remain poorly understood. In this study, we report our analysis of the role of the Ets transcription factor, Spi-B, in this process. Spi-B expression is acutely induced coincident with T cell lineage commitment at the CD4(-)CD8(-)CD44(-)CD25(+) (DN3) stage of thymocyte development and is then down-regulated as thymocytes respond to pre-TCR signals and develop beyond the beta-selection checkpoint to the CD4(-)CD8(-)CD44(-)CD25(-) (DN4) stage. We found that dysregulation of Spi-B expression in DN3 thymocytes resulted in a dose-dependent perturbation of thymocyte development. Indeed, DN3 thymocytes expressing approximately five times the endogenous level of Spi-B were arrested at the beta-selection checkpoint, due to impaired induction of Egr proteins, which are important molecular effectors of the beta-selection checkpoint. T lineage-committed DN3 thymocytes expressing even higher levels of Spi-B were diverted to the dendritic cell lineage. Thus, we demonstrate that the prescribed modulation of Spi-B expression is important for T lineage commitment and differentiation beyond the beta-selection checkpoint; and we provide insight into the mechanism underlying perturbation of development when that expression pattern is disrupted.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Differentiation / genetics*
  • Cell Differentiation / immunology*
  • Cell Line, Tumor
  • Cell Lineage / genetics
  • Cell Lineage / immunology
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / deficiency
  • DNA-Binding Proteins / genetics
  • Dendritic Cells / cytology
  • Dendritic Cells / immunology
  • Down-Regulation / genetics
  • Down-Regulation / immunology*
  • Fetal Development / genetics
  • Fetal Development / immunology
  • Genes, T-Cell Receptor beta / immunology*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, SCID
  • Organ Culture Techniques
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins / deficiency
  • Proto-Oncogene Proteins / genetics*
  • T-Lymphocyte Subsets / cytology*
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism*
  • Thymoma / genetics
  • Thymoma / immunology
  • Thymus Gland / cytology
  • Thymus Gland / immunology
  • Thymus Gland / metabolism
  • Thymus Neoplasms / genetics
  • Thymus Neoplasms / immunology
  • Trans-Activators / biosynthesis*
  • Trans-Activators / deficiency
  • Trans-Activators / genetics*
  • Transcription Factors / biosynthesis
  • Transcription Factors / deficiency
  • Transcription Factors / genetics
  • Transduction, Genetic

Substances

  • DNA-Binding Proteins
  • Ehf protein, mouse
  • Proto-Oncogene Proteins
  • Trans-Activators
  • Transcription Factors
  • proto-oncogene protein Spi-1
  • SPIB protein, human