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Mechanisms of Graft-vs.-Leukemia against a Novel Murine Model of Chronic Myelogenous Leukemia

机译:移植物抗白血病对新型慢性粒细胞白血病小鼠模型的作用机制

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Our objective is to understand the immunobiology underlying the differential sensitivity of chronic phase and blast crisis CML. Our data thus far support the hypothesis that GVL against mCP-CML can be mediated by redundant processes and that impairment of an individual pathway is insufficient to prevent GVL. We hypothesize that GVL against BC-CML is less forgiving than that against CP-CML, and that multiple effector pathways must act in concert for effective GVL. In the last year we have: (1) determined that cognate interactions are required for 0D4 and 0D8-mediated GVL; (2) determined that host antigen presenting cells are required for both 0D4 and 0D8-mediated GVL; (3) determined that killing by either FasL or TNF-o is not required for 0D4 or 0D8-mediated GVL; (4) created B7H14- mBC-CML; (5) determined that B7Hi expressed on mBC-CML does not impede 0D8-mediated GVL; (6) created TGF-p4- mBC- CML; and (7) determined that effector memory 0D4 cells can mediate GVL against mBC-CML.

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