American Society of Hematology

Figure 3.

$Figure 3. Stat1−/− mice recapitulate the phenotype of coexisting MPN and B-cell transformation. (A) BM of Stat1−/− mice with 6 weeks of age (n = 3), 4 months of age (n = 3), and Stat1−/− MPN+ mice (n = 6) was analyzed for D-J rearrangement of the IgH gene. Pc, polyclonal B cells (derived from splenocytes of a wt mouse). Asterisks denote samples of those mice, whose B-cell clonality was followed in subsequent transplantations (outlined in supplemental Figure 5C). (B) BMs or spleens of MPN+ Stat1−/− mice were fractionated into LSK (Lin− Sca-1+c-Kit+), progenitors (Lin− c-Kit+Sca-1−), CD3+, Mac1+, Gr1+Mac1+, CD19+, and Lin+ cells and intravenous injected into Rag2−/−γc−/− mice. Table shows incidence of B-cell disease in recipient mice that had received individual populations or whole BM. (C) Cytospins of Stat1−/− B-cell lines: #503, #1762, #6500 and #7473. Original magnification: 40×. Scale bar, 10 μm.$

Stat1^−/−mice recapitulate the phenotype of coexisting MPN and B-cell transformation. (A) BM of Stat1^−/− mice with 6 weeks of age (n = 3), 4 months of age (n = 3), and Stat1^−/− MPN⁺ mice (n = 6) was analyzed for D-J rearrangement of the IgH gene. Pc, polyclonal B cells (derived from splenocytes of a wt mouse). Asterisks denote samples of those mice, whose B-cell clonality was followed in subsequent transplantations (outlined in supplemental Figure 5C). (B) BMs or spleens of MPN⁺Stat1^−/− mice were fractionated into LSK (Lin⁻ Sca-1⁺c-Kit⁺), progenitors (Lin⁻ c-Kit⁺Sca-1⁻), CD3⁺, Mac1⁺, Gr1⁺Mac1⁺, CD19⁺, and Lin⁺ cells and intravenous injected into Rag2^−/−γc^−/− mice. Table shows incidence of B-cell disease in recipient mice that had received individual populations or whole BM. (C) Cytospins of Stat1^−/− B-cell lines: #503, #1762, #6500 and #7473. Original magnification: 40×. Scale bar, 10 μm.

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