Figure 1.
Figure 1. LCs develop from myeloid progenitors after UV light-induced skin inflammation. (A) Transplantation model. Lethally irradiated CD45.2 C57Bl/6 mice were injected intravenously with progenitor cells isolated from congenic CD45.1 mice plus 105 CD45.2 BM cells to ensure survival. Twenty-four hours after progenitor transplantation, mice received 20 minutes of UV light treatment to recruit progenitor cells to the skin. LC chimerism was analyzed by flow cytometry of epidermal cells. (B) Histogram plots show CD45.1 expression of epidermal cells isolated from mice 2 weeks after transplantation with 104 CMPs or 4 × 104 GMPs, or control mice. Control mice received transplants of autologous support BM cells only. Contour plots show CD11c/I-Ab expression profile of gated CD45.1+ and CD45.1- epidermal cells. Percentages of LCs derived from host- or donor-derived cells are indicated. Data are representative of at least 5 mice that underwent transplantation per progenitor population.

LCs develop from myeloid progenitors after UV light-induced skin inflammation. (A) Transplantation model. Lethally irradiated CD45.2 C57Bl/6 mice were injected intravenously with progenitor cells isolated from congenic CD45.1 mice plus 105 CD45.2 BM cells to ensure survival. Twenty-four hours after progenitor transplantation, mice received 20 minutes of UV light treatment to recruit progenitor cells to the skin. LC chimerism was analyzed by flow cytometry of epidermal cells. (B) Histogram plots show CD45.1 expression of epidermal cells isolated from mice 2 weeks after transplantation with 104 CMPs or 4 × 104 GMPs, or control mice. Control mice received transplants of autologous support BM cells only. Contour plots show CD11c/I-Ab expression profile of gated CD45.1+ and CD45.1- epidermal cells. Percentages of LCs derived from host- or donor-derived cells are indicated. Data are representative of at least 5 mice that underwent transplantation per progenitor population.

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