Figure 5.
In vitro expanded Tregs suppress GVHD in NSG-SGM3 mice. (A) Schematic representation of isolation of Tregs, followed by xenotransplantation and downstream analysis. (B) Measurement of body weight loss (representing GVHD disease clinical feature) in recipient mice that were injected with HD-derived PBMCs without (n = 14) or with Tregs (autologous or allogenic) (n = 9) or Tregs alone (n = 3). (C) Overall survival of mice that were injected with HD-derived PBMCs without (n = 14) or with Tregs (autologous or allogenic) (n = 9) or Tregs alone (n = 3). (D) Representative histology tissue sections of the mouse femur bone and spleen. Hematoxylin and eosin staining; scale bar, 100 μm. (E) Overall survival of mice that were injected with AA patient-derived PBMCs without (n = 5) or with AA Tregs (autologous or allogenic) (n = 8) or AA Tregs alone (n = 2).

In vitro expanded Tregs suppress GVHD in NSG-SGM3 mice. (A) Schematic representation of isolation of Tregs, followed by xenotransplantation and downstream analysis. (B) Measurement of body weight loss (representing GVHD disease clinical feature) in recipient mice that were injected with HD-derived PBMCs without (n = 14) or with Tregs (autologous or allogenic) (n = 9) or Tregs alone (n = 3). (C) Overall survival of mice that were injected with HD-derived PBMCs without (n = 14) or with Tregs (autologous or allogenic) (n = 9) or Tregs alone (n = 3). (D) Representative histology tissue sections of the mouse femur bone and spleen. Hematoxylin and eosin staining; scale bar, 100 μm. (E) Overall survival of mice that were injected with AA patient-derived PBMCs without (n = 5) or with AA Tregs (autologous or allogenic) (n = 8) or AA Tregs alone (n = 2).

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