A reversible defect in alpha-beta T cell receptor assembly

Exp Cell Res. 1996 Feb 25;223(1):149-54. doi: 10.1006/excr.1996.0068.

Abstract

A human leukemia cell line, SUP-T13, can gain and lose TCR/CD3 expression at rates incompatible with spontaneous mutation. In this study, we determined (i) the generality of this phenomenon among other T cell lines, (ii) the specificity of this phenomenon to the TCR/CD3 complex, and (iii) the molecular mechanism of TCR/CD3 loss in the SUP-T13 cell line at a biochemical level. We show that two other T cell lines can undergo gain and loss of TCR/CD3 expression at similar rates. However, class I MHC molecules do not switch expression on and off, demonstrating that such switching is not an artifact of the analysis. To determine the mechanism for loss of surface TCR/CD3 expression, pulse-chase labeling and immunoprecipitation were performed on SUP-T13 TCR/CD3 negative cells. These analyses revealed that TCR alpha proteins are produced, but do not covalently associate with TCR beta-CD3 proteins in the negative cells. Thus, these variants represent a novel level of posttranslational regulation of TCR/CD3 expression, namely, the disulfide linkage of alpha and beta TCR chains.

MeSH terms

  • Glycosylation
  • Humans
  • Leukemia, T-Cell
  • Protein Conformation
  • Protein Processing, Post-Translational
  • Receptor-CD3 Complex, Antigen, T-Cell / biosynthesis*
  • Receptor-CD3 Complex, Antigen, T-Cell / metabolism
  • Receptors, Antigen, T-Cell, alpha-beta / biosynthesis*
  • Receptors, Antigen, T-Cell, alpha-beta / chemistry
  • Receptors, Antigen, T-Cell, alpha-beta / metabolism
  • T-Lymphocytes / immunology*
  • Tumor Cells, Cultured

Substances

  • Receptor-CD3 Complex, Antigen, T-Cell
  • Receptors, Antigen, T-Cell, alpha-beta