Figure 2
Figure 2. Mushi1 and 2 mice develop histiocytosis. (A) The high and low Tg-expressing Mushi1 and Mushi2 lines show an early and late development of disease signs (anemia and general symptoms), respectively. (B) Hematocrit values in percentage of healthy control (LM) and diseased Mushi1 mice (Tg). (C) Multiple nodules and organ enlargement in spleen, liver, and mesenteric LN (MLN) from diseased mice (Mushi1) compared with healthy controls (LM). (D) Similar histologic characteristics in human LCH in LN (human) and Mushi1 liver lesions (TG) are detected by hematoxylin & eosin (H&E) and immunostaining for Langerin (CD207) and S100. (E) Human and Mushi lesions show reniform nuclei (enlargement of D left column). (F) Expression of the cell cycle marker Ki-67 was tested by FACS in gated CD11cāˆ’ and CD11c+ MLN cells from control (LM) and diseased (TG) mice. (G) Normal human spleen stained with anti-CD1a or anti-Langerin antibodies.

Mushi1 and 2 mice develop histiocytosis. (A) The high and low Tg-expressing Mushi1 and Mushi2 lines show an early and late development of disease signs (anemia and general symptoms), respectively. (B) Hematocrit values in percentage of healthy control (LM) and diseased Mushi1 mice (Tg). (C) Multiple nodules and organ enlargement in spleen, liver, and mesenteric LN (MLN) from diseased mice (Mushi1) compared with healthy controls (LM). (D) Similar histologic characteristics in human LCH in LN (human) and Mushi1 liver lesions (TG) are detected by hematoxylin & eosin (H&E) and immunostaining for Langerin (CD207) and S100. (E) Human and Mushi lesions show reniform nuclei (enlargement of D left column). (F) Expression of the cell cycle marker Ki-67 was tested by FACS in gated CD11cāˆ’ and CD11c+ MLN cells from control (LM) and diseased (TG) mice. (G) Normal human spleen stained with anti-CD1a or anti-Langerin antibodies.

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