Fig. 9.
Fig. 9. Engrafted mice showed no evidence of characteristic sickle splenic and renal pathology. / (A,B) Histology of the spleen in untreated and engrafted mice. (A) Untreated sickle spleen. Splenic architecture is highly abnormal with pooling of sickled RBCs and areas of increased hematopoiesis. (B) Spleen from an engrafted mouse killed 5 months after transplantation. Splenic architecture is now normal. No RBC pooling is present. (C,D) Histology of the kidney in untreated and engrafted mice. (C) Untreated sickle kidney. The sickle kidney shows evidence of membranoproliferative glomerulonephritis. Arrowheads point to thickened glomerular membrane. Arrows point to narrowed glomerular space. (C) Kidney from an engrafted mouse killed 5 months after transplantation. Glomerular architecture is now normal. Sickle mice were age-matched to engrafted mice for this analysis. Sections were stained with hematoxylin and eosin. Bars = 50 μm.

Engrafted mice showed no evidence of characteristic sickle splenic and renal pathology.

(A,B) Histology of the spleen in untreated and engrafted mice. (A) Untreated sickle spleen. Splenic architecture is highly abnormal with pooling of sickled RBCs and areas of increased hematopoiesis. (B) Spleen from an engrafted mouse killed 5 months after transplantation. Splenic architecture is now normal. No RBC pooling is present. (C,D) Histology of the kidney in untreated and engrafted mice. (C) Untreated sickle kidney. The sickle kidney shows evidence of membranoproliferative glomerulonephritis. Arrowheads point to thickened glomerular membrane. Arrows point to narrowed glomerular space. (C) Kidney from an engrafted mouse killed 5 months after transplantation. Glomerular architecture is now normal. Sickle mice were age-matched to engrafted mice for this analysis. Sections were stained with hematoxylin and eosin. Bars = 50 μm.

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