Fig. 8.
Fig. 8. Histopathological studies of spleens from wild-type, L-selectin–deficient, E/P double-selectin–null, and E/L/P triple-selectin–null mice. / (A) The normal red and white pulp architecture of the spleen was present in control mice (n = 6). (B) Splenic architecture was distorted by extramedullary hematopoiesis in L-selectin–deficient mice (n = 6); however, this was to a much lesser extent than in the E/P-selectin– and E/L/P-selectin–null mice. Extramedullary hematopoiesis in spleens was markedly increased in the E/P-selectin (C) and E/L/P-selectin (D) null mice. The architectural disorganization was much more pronounced in the E/P double-mutant mice (n = 12) than in the triple-selectin–null mice (n = 6; hematoxylin and eosin, original magnification × 200).

Histopathological studies of spleens from wild-type, L-selectin–deficient, E/P double-selectin–null, and E/L/P triple-selectin–null mice.

(A) The normal red and white pulp architecture of the spleen was present in control mice (n = 6). (B) Splenic architecture was distorted by extramedullary hematopoiesis in L-selectin–deficient mice (n = 6); however, this was to a much lesser extent than in the E/P-selectin– and E/L/P-selectin–null mice. Extramedullary hematopoiesis in spleens was markedly increased in the E/P-selectin (C) and E/L/P-selectin (D) null mice. The architectural disorganization was much more pronounced in the E/P double-mutant mice (n = 12) than in the triple-selectin–null mice (n = 6; hematoxylin and eosin, original magnification × 200).

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