کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2139250 | 1087898 | 2007 | 7 صفحه PDF | دانلود رایگان |
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-γ 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.
Journal: Leukemia Research - Volume 31, Issue 12, December 2007, Pages 1675–1681