A small population of cells in acute lymphoblastic leukaemia is characteriz
ed by a specific translocation of the c-nhl oncogene on chromosome 9 to the
break point cluster lesion (bcr) on chromosome 22, t(9;22)(q34;q11) (e1a2)
. Theoretically, the junction-spanning sequences of oncogene fusion protein
s might be ideal targets for immunotherapy because these are not present in
normal cells. In this study, we show for the first time that in vitro immu
nization with a 17-mer e1a2 peptide representing the p190 minor bcr-abl fus
ion protein resulted in HLA-DRB1*1501-restricted peptide-specific prolifera
tive CD4(+) T lymphocytes, using peptide-pulsed monocyte-derived dendritic
cells as the antigen-presenting cells.