Activation of cord T lymphocytes. II. Cellular and molecular analysis of the defective response induced by anti-CD3 monoclonal antibody

Alberto Bertotto, Roberto Gerli, Luisa Lanfrancone, Silvana Crupi, Carla Arcangeli, Cristina Cernetti, Fabrizio Spinozzi, Pietro Rambotti

Research output: Contribution to journalArticle

Abstract

Despite the fact that the percentage of circulating CDS-positive cells is similar in cord and adult blood, the proliferative response induced by anti-CD3 monoclonal antibody (mAb) was impaired in the majority of human cord peripheral blood mononuclear cell (PBMC) samples we tested. The cell proliferative defect was associated with low interleukin 2 (IL 2) gene expression and scant IL 2 production. However, interleukin 2 receptor was fully expressed at both the mRNA and protein levels. Such a finding is consistent with the observation that exogenous recombinant IL 2 is able to boost the anti-CD3-mediated response of cord PBMC. Furthermore, when anti-CD3 and phorbol myristate acetate (PMA) were added together, they exerted a very marked synergistic effect on both the proliferation of, and IL 2 production by, cord PBMC. The addition of allogeneic antigen presenting cells plus soluble anti-CD3 or Sepharose-coupled anti-CD3 mAb to the cord T cell cultures had no significant effect on proliferation, whereas both elicited good mitogenesis of adult T cells. Moreover, addition of exogenous recombinant inter-leukin 1 to anti-CDS-stimulated T cells failed to trigger any proliferation in either adult or cord samples. Since the combination of PMA and calcium ionophore A23187 is effective in triggering optimal proliferation of cord T cells, the defect would seem to be associated with a failure in transmembrane transduction of the activation signals provided by the anti-CD3 stimulus for the cord T Cell.

Original languageEnglish
Pages (from-to)247-259
Number of pages13
JournalCellular Immunology
Volume127
Issue number2
DOIs
Publication statusPublished - 1990

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ASJC Scopus subject areas

  • Cell Biology
  • Immunology

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