GvL is more pronounced in MHC-mismatched than in MHC-matched, miHA-mismatched chimeras. (A-B) Plot of PBL counts (A) and percentage of allogeneic chimerism (B) as a function of time after BMT (x-axis) for MHC-mismatched (red triangles) and MHC-matched, miHA-mismatched (blue diamonds) chimeras with CML-like leukemia treated with DLI. Note that in the miHA-mismatched setting, because of the predominance of the syngeneic BCR-ABL–transduced BM, allogeneic chimerism never rose above 40%. (C) Flow cytometric analysis of allogeneic chimerism (y-axis, detecting the β₂-microglobulin^b allele expressed by B10.D2 leukocytes) and level of GFP⁺ leukemia cells (x-axis) in sequential peripheral blood samples from a representative mouse with MHC-matched, miHA-mismatched mixed chimerism and CML-like disease treated with DLI. The mouse was treated on days 15, 17, and 21 with a total dose of 1.1 × 10⁸ B10.D2 splenocytes; note the increasing population of circulating GFP⁺ leukemia cells and diminishing allogeneic chimerism from 33% on day 14 to 15% on day 20. (D) Allotypic specificity of Cy-Chrome–labeled antibody against β₂-microglobulin^b (y-axis). Flow cytometric plots of PBLs from Balb/c mice stained with Cy-Chrome–labeled isotype control antibody (left panel) and PBLs from Balb/c (middle panel) or B10.D2 (right panel) mice stained with Cy-Chrome–labeled anti–β₂-microglobulin^b antibody. (E-F) Cumulative leukemic mortality (E) and overall survival (F) for DLI-treated recipients of TCD BCR-ABL–transduced Balb/c BM and TCD B6 BM (MHC-mismatch + DLI; red, n = 7) and for recipients of TCD BCR-ABL–transduced Balb/c BM and TCD B10.D2 BM (miHA-mismatch) with (blue, n = 7) or without (gray, n = 4) DLI treatment.