Mechanisms of Graft-vs.-Leukemia against a Novel Murine Model of Chronic Myelogenous Leukemia
Final rept. 1 Jul 2003-30 Jun 2006
YALE UNIV NEW HAVEN CT SCHOOL OF MEDICINE
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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.
- Anatomy and Physiology
- Medicine and Medical Research