Fig. 3.
Fig. 3. Comparison of the histopathology of CML-like disease in different cytokine-deficient backgrounds. / Photomicrographs of hematoxylin/eosin-stained sections (magnification × 100) of spleen (A,D,G,J) and liver (B,E,H,K), and Wright/Giemsa-stained smears (magnification × 400) of peripheral blood (C,F,I,L), from mice with BCR/ABL-induced myeloproliferative disease where donor and recipient were of wild-type (A-C), Il-3−/− (D-F),Gm-csf−/− (G-I), and double-knockout (J-L) genotypes. Spleens demonstrate complete disruption of follicular architecture by infiltrating myeloid cells, erythropoiesis, and megakaryocytosis. Livers exhibit sinusoidal infiltration with maturing neutrophils, extramedullary erythropoiesis, and periportal collections of macrophages. Peripheral blood of mostIl-3−/− and some double-knockout recipients of like marrow displayed a predominance of monocytes and macrophages rather than neutrophils.

Comparison of the histopathology of CML-like disease in different cytokine-deficient backgrounds.

Photomicrographs of hematoxylin/eosin-stained sections (magnification × 100) of spleen (A,D,G,J) and liver (B,E,H,K), and Wright/Giemsa-stained smears (magnification × 400) of peripheral blood (C,F,I,L), from mice with BCR/ABL-induced myeloproliferative disease where donor and recipient were of wild-type (A-C), Il-3−/− (D-F),Gm-csf−/− (G-I), and double-knockout (J-L) genotypes. Spleens demonstrate complete disruption of follicular architecture by infiltrating myeloid cells, erythropoiesis, and megakaryocytosis. Livers exhibit sinusoidal infiltration with maturing neutrophils, extramedullary erythropoiesis, and periportal collections of macrophages. Peripheral blood of mostIl-3−/− and some double-knockout recipients of like marrow displayed a predominance of monocytes and macrophages rather than neutrophils.

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