Pharmacologic suppression of target cell recognition by engineered T cells expressing chimeric T-cell receptors

Cancer Gene Ther. 2000 Apr;7(4):526-9. doi: 10.1038/sj.cgt.7700128.

Abstract

Adoptive therapy with autologous T cells expressing chimeric T-cell receptors (chTCRs) is of potential interest for the treatment of malignancy. To limit possible T-cell-mediated damage to normal tissues that weakly express the targeted tumor antigen (Ag), we have tested a strategy for the suppression of target cell recognition by engineered T cells. Jurkat T cells were transduced with an anti-hapten chTCR tinder the control of a tetracycline-suppressible promoter and were shown to respond to Ag-positive (hapten-coated) but not to Ag-negative target cells. The engineered T cells were then reacted with hapten-coated target cells at different effector to target cell ratios before and after exposure to tetracycline. When the engineered T cells were treated with tetracycline, expression of the chTCR was greatly decreased and recognition of the hapten-coated target cells was completely suppressed. Tetracycline-mediated suppression of target cell recognition by engineered T cells may be a useful strategy to limit the toxicity of the approach to cancer gene therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Flow Cytometry
  • Haptens / pharmacology
  • HeLa Cells
  • Humans
  • Interleukin-2 / biosynthesis
  • Jurkat Cells
  • Lymphocyte Activation* / drug effects
  • Nitrohydroxyiodophenylacetate / pharmacology*
  • Receptors, Antigen, T-Cell / genetics*
  • Receptors, Antigen, T-Cell / immunology*
  • Recombinant Fusion Proteins / biosynthesis
  • Recombinant Fusion Proteins / immunology
  • T-Lymphocytes / immunology*
  • Tetracycline / pharmacology
  • Transfection*

Substances

  • Haptens
  • Interleukin-2
  • Receptors, Antigen, T-Cell
  • Recombinant Fusion Proteins
  • Nitrohydroxyiodophenylacetate
  • Tetracycline