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 BC-CML in B6 mice and have established the basic features of the model: 1) survival versus cell dose; 2) that GVL requires alloantigen differences; 3) that GVL can be mediated by unfractionated lymph node cells; 4) that GVL can be mediated by purified CD4 or CD8 cells, but that large doses are required. We are currently creating gene-deficient BC-CML and anticipate rapid progress this year in identifying key effector mechanisms and modes of antigen presentation.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2004
- Accession Number
- ADA426337
Entities
People
- Warren D. Shlomchik
Organizations
- Yale University