Evidence that a BCR-ABL fusion peptide does not induce lymphocyte proliferation or cytokine production in vitro
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Updated: Jul 16, 2026

Isolation and Activation of Murine Lymphocytes
Published on: October 30, 2016
Hazem M Abu-Eisha1, Nauman M Butt, Richard E Clark
1Division of Immunology, University of Liverpool, UK.
Abstract:
The BCR-ABL fusion protein is characteristic of chronic myeloid leukaemia and may be an effective tumour-specific antigen. CD8+ T cell responses to BCR-ABL fusion peptides have been reported in normal subjects and CML patients but CD4+ T cell responses have been less well characterised. Here, the 23-mer e14a2 fusion peptide VHSATGFKQSSKALQRPVASDFE has been used to stimulate T cell responses. Most normal subjects and CML patients showed no proliferative responses to this peptide, with stimulation indices not significantly greater than 1.0. Following a second stimulation with the same peptide, small proliferative responses were obtained in normal subjects but not CML patients. These responses were not improved following a third stimulation with 23-mer peptide, nor by using mature autologous dendritic cells to present the peptide. Intracellular interferon-gamma production by CD4+ T cells was also not induced by the 23-mer e14a2 peptide. Hence, this e14a2 peptide does not stimulate CD4+ T cell proliferation in vitro in most normal subjects or CML patients. The precise sequence of amino acids may be critical in defining immunogenicity for CD4+ T cell responses against BCR-ABL peptides.
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