Successful immunotherapy of CML-like leukemia is complicated by GvHD with ascites and by graft failure. (A) Plot of body weight in grams (y-axis) as a function of time after BMT for the recipients in Figure 2E, showing chimeric mice treated with DLI (red) and mice that received allogeneic splenocytes at BMT (green). (B) Wright-Giemsa stain of histiocytic cells in ascites from a representative mixed chimeric mouse with CML-like leukemia that developed GvHD after DLI (magnification × 400). (C-G) Flow cytometric analysis of ascitic fluid from panel B. Analysis of GFP expression (x-axis) versus the macrophage markers Mac-1 (C), Mac-3 (D), and F4/80 (E), and MHC class I antigens H-2^b (F) and H-2^d (G). Note that H-2^b+/H-2^d- histiocytic cells express macrophage markers and low levels of GFP. (H) PB leukocytes from this mouse, analyzed for expression of Mac-1 (y-axis) and GFP (x-axis). Note that circulating GFP⁺ myeloid cells have been eradicated. (I) Analysis of chimerism (top row) and CML-like leukemia (bottom row) in a mixed chimera that developed pancytopenia following successful DLI. On day 31, the PB hemoglobin was 48 g/L (4.8 g/dL) and platelet count was 213 ×10⁹/L (213 000/μL). (J) Hematoxylin and eosin (H&E)–stained bone marrow section from a representative mouse with pancytopenia after DLI, showing severe cellular hypoplasia (magnification × 150).