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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 286-293
HLA class I-restricted lysis of leukemia cells by a
CD8+ cytotoxic T-lymphocyte clone specific for WT1
peptide
Hideki Ohminami,
Masaki Yasukawa, and
Shigeru Fujita
From the First Department of Internal Medicine, Ehime University
School of Medicine, Shigenobu, Ehime, Japan.
The Wilms tumor (WT1) gene has been reported to be
preferentially expressed in acute leukemia cells, regardless of
leukemia subtype and chronic myelogenous leukemia cells in blast
crisis, but not in normal cells. This finding suggests strongly that
WT1 protein is a potential target of immunotherapy for human leukemia. In this study, we established a CD8+ cytotoxic
T-lymphocyte (CTL) clone directed against a WT1-derived peptide and
examined its immunologic actions on leukemia cells. A
CD8+ CTL clone, designated TAK-1, which lysed
autologous cells loaded with a WT1-derived 9-mer peptide
consisting of the HLA-A24 (HLA-A*2402)-binding motifs was established
by stimulating CD8+ T lymphocytes from a healthy
individual repeatedly with WT1 peptide-pulsed autologous dendritic
cells. TAK-1 was cytotoxic to HLA-A24-positive leukemia cells
expressing WT1, but not to HLA-A24-positive lymphoma cells that did
not express WT1, HLA-A24-negative leukemia cells, or HLA-A24-positive
normal cells. Treating leukemia cells with an antisense oligonucleotide
complementary to the WT1 gene resulted in reduced
TAK-1-mediated cytotoxicity, suggesting that target antigen of TAK-1 on
leukemia cells is the naturally processed WT1 peptide in the context of
HLA-A24. TAK-1 did not inhibit colony formation by normal bone marrow
cells of HLA-A24-positive individuals. Because WT1 is overexpressed
ubiquitously in various types of leukemia cells, but not in normal
cells, immunotherapy using WT1 peptide-specific CTL clones should be an
efficacious treatment for human leukemia. (Blood. 2000;95:286-293)
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