Chronic myeloid leukemia (CML) is characterized by a specific transloc
ation of the c-abl oncogene on chromosome 9 to the break point cluster
region (bcr) on chromosome 22, t(9;22) (q34;q11). This translocation
results in the expression of a 210-kD bcr-abl protein fusion gene prod
uct. The juxtaposition of the bcr and abl genes produces a novel junct
ional amino acid sequence, which may be presented by antigen-presentin
g cells and recognized specifically by human T lymphocytes, We have ge
nerated a CD4(+) T lymphocyte line (NG-1) which recognizes the peptide
epitope (GFKQSSKALQR) in association with HLA-DR beta 10101-02, A co
mparison of antigen-presenting cells showed that CMRF-44(+) blood dend
ritic cell presented a 12mer b3a2 peptide effectively, The b3a2 peptid
e was able to generate specific primary T-lymphocyte responses in othe
r HLA-DR1 donors. We also show that bcr-abl, b3a2 peptide-specific T-l
ymphocyte lines proliferate in response to bcr-abl b3a2 containing cel
l lysates (K562 or CML PBMC derived) but not control (including b2a2 C
ML PBMC) lysates. (C) 1997 by The American Society of Hematology.