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| ROLE OF B7-1 IN MEDIATING AN IMMUNE-RESPONSE TO MYELOID-LEUKEMIA CELLS |
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| Author(s): MATULONIS UA, DOSIOU C, LAMONT C, FREEMAN GJ, MAUCH P, NADLER LM, GRIFFIN JD |
| Source: BLOOD Volume: 85 Issue: 9 Pages: 2507-2515 Published: MAY 1 1995 |
| Times Cited: 116 References: 49 |
| Abstract: 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. (C) 1995 by The American Society of Hematology. |
| Document Type: Article |
| Language: English |
| Reprint Address: MATULONIS, UA (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV HEMATOL MALIGNANCIES, 44 BINNEY ST, BOSTON, MA 02115 USA |
| Publisher: W B SAUNDERS CO, INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 |
| Subject Category: Hematology |
| IDS Number: QW602 |
| ISSN: 0006-4971 |
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