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The use of HLA A2.1/p53 peptide tetramers to visualize the impact of self tolerance on the TCR repertoire

Academic Article
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Overview

authors

  • Hernandez, J.
  • Lee, Pauline
  • Davis, M. M.
  • Sherman, Linda

publication date

  • January 2000

journal

  • Journal of Immunology  Journal

abstract

  • p53 is an attractive target for cancer immunotherapy since it is overexpressed in half of all tumors. However, it is also expressed in normal lymphoid tissue, and self tolerance leaves a p53-specific repertoire purged of high avidity CTL. To better understand the mechanism of tolerance and the basis for such low avidity interaction, p53-specific CTL from p53 deficient (p53-) and sufficient (p53+) A2.1/Kb transgenic mice were compared with respect to their ability to bind HLA-A2.1 tetramers containing cognate murine p53 peptide Ag, p53 261-269. Since the murine CD8 molecule cannot interact with human HLA-A2.1, this tests the ability of the TCR to bind the A2.1/peptide complex tetramer. CTL from p53- mice demonstrated strong binding of such A2.1/p53 261-269 tetramers; however, the CTL from tolerant p53+ mice were devoid of tetramer-binding CD8+ T cells. Examination of TCR expression at the clonal level revealed that CTL from p53+ and p53- mice each expressed comparable levels of the p53-specific TCR. These results indicate that normal expression of p53 promotes elimination of T cells expressing TCRs with sufficient affinity to achieve stable binding of the A2.1/p53 261-269 tetramers.

subject areas

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Binding Sites
  • Cell Line
  • Clone Cells
  • H-2 Antigens
  • HLA-A2 Antigen
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Molecular Sequence Data
  • Peptide Fragments
  • Receptors, Antigen, T-Cell, alpha-beta
  • Self Tolerance
  • T-Lymphocytes, Cytotoxic
  • Tumor Suppressor Protein p53
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 10623800
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Additional Document Info

start page

  • 596

end page

  • 602

volume

  • 164

issue

  • 2

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