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: 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 cell:leukemia 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.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2005
- Accession Number
- ADA443726
Entities
People
- Warren D. Shlomchik
Organizations
- Yale University