作者: UA Matulonis , C Dosiou , C Lamont , GJ Freeman , P Mauch
DOI: 10.1182/BLOOD.V85.9.2507.BLOODJOURNAL8592507
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摘要: 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 contribute the failure immune recognition these diseases. murine leukemia model system was developed assess potential role in induction immunity cells. The nonleukemic 32Dc13 myeloid cell line transformed by transfection BCR/ABL gene, generating a subline (32Dp210/clone 26) that leukemic rapidly lethal syngeneic, immunocompetent C3H/HeJ mice or T-cell-deficient nude mice. B7-1-modified cells remained mice, but caused only transient, nonlethal After single exposure live, nonirradiated cells, protective against subsequent challenge with B7-1(-) Further, hyperimmunization B7-1(+) prolonged survival previously injected number These results indicate may be attractive candidates gene transfer.