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Role of B7-1 in mediating an immune response to myeloid leukemia cells
UA Matulonis, C Dosiou, C Lamont, GJ Freeman, P Mauch, LM Nadler and JD Griffin
Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston,
MA 02115, USA.
A costimulatory signal from B7-1 (CD80) to its counter-receptor CD28 is
required for T-cell activation. Many tumors, including most human
leukemias, lack expression of B7-1, and this has been suggested to
contribute to the failure of immune recognition of these diseases. A murine
leukemia model system was developed to assess the potential role of B7-1 in
the induction immunity to leukemia cells. The nonleukemic 32Dc13 myeloid
cell line was transformed by transfection of the BCR/ABL gene, generating a
subline (32Dp210/clone 26) that was leukemic and rapidly lethal to
syngeneic, immunocompetent C3H/HeJ mice or T-cell- deficient nude mice.
B7-1-modified leukemic cells remained lethal in nude mice, but caused only
a transient, nonlethal leukemia in C3H/HeJ mice. After a single exposure to
live, nonirradiated B7-1-modified leukemic cells, C3H/HeJ mice developed
protective immunity against subsequent challenge with B7-1(-) leukemic
cells. Further, hyperimmunization with B7-1(+) leukemic cells prolonged the
survival of mice previously injected with a lethal number of B7-1(-)
leukemic cells. These results indicate that myeloid leukemic cells may be
attractive candidates for B7-1 gene transfer.
Volume 85,
Issue 9,
pp. 2507-2515,
05/01/1995
Copyright © 1995 by The American Society of Hematology
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