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PubMed · 8635487

A reversible defect in alpha-beta T cell receptor assembly.

H Maecker·J T Thomas·R L Consorti·T M Ellis
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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.

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GlycosylationHumansLeukemia, T-CellProtein ConformationProtein Processing, Post-TranslationalReceptor-CD3 Complex, Antigen, T-CellReceptors, Antigen, T-Cell, alpha-betaT-LymphocytesTumor Cells, CulturedJournal Article

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H Maecker, J T Thomas, R L Consorti, T M Ellis. 1996-02-25. A reversible defect in alpha-beta T cell receptor assembly.. https://doi.org/10.1006/excr.1996.0068

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