Mechanisms of Graft-vs.-Leukemia against a Novel Murine Model of Chronic Myelogenous Leukemia
Abstract
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.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2006
- Accession Number
- ADA464064
Entities
People
- Warren D. Shlomchik
Organizations
- Yale University