Mechanisms of Graft-vs.-Leukemia Against a Novel Murine Model of Chronic Myelogenous Leukemia
Annual rept. 1 Jul 2004-30 Jun 2005
YALE UNIV NEW HAVEN CT
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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 created multiple gene deficient mBC-CMLs cloned these and established clonality by southern blot analysis assessed whether host APCs are required for CD4 and CD8-mediated GVL determined that cognate T cellleukemia interactions are required for CD4 and CD8-mediated GVL determined that mBC-CML cells express high levels of B7-H1-- obtained B7-H1 gene deficient mice to create B7-H1-- mBC-CML and begun a new collaboration to study the role of TGF-Beta in mBC-CML GVL resistance.
- Medicine and Medical Research