Fig. 3: Overexpression of Peli1 in epidermal cells but not in T cells triggers the development of psoriasis-like disease. | Experimental & Molecular Medicine

Fig. 3: Overexpression of Peli1 in epidermal cells but not in T cells triggers the development of psoriasis-like disease.

From: Pellino1 promotes chronic inflammatory skin disease via keratinocyte hyperproliferation and induction of the T helper 17 response

Fig. 3

a, b Schematic representation of the generation of chimeric recipient mice. Bone marrow (BM) cells were isolated from donor mice and injected into lethally irradiated recipient mice. The following four groups were generated: Pepboy.1 (CD45.1) BM →rtTA (CD45.2) mice (group 1); Pepboy.1 (CD45.1) BM → rtTA-Peli1 (CD45.2) mice (group 2); rtTA (CD45.2) BM → Pepboy.1 (CD45.1) mice (group 3); and rtTA-Peli1 (CD45.2) BM → Pepboy.1 (CD45.1) mice (group 4). After BMT, each group of mice was treated with doxycycline for 12 weeks and then sacrificed (n = 3 for each group). c, e H&E-stained sections of skin from each group of mice treated with doxycycline for 12 weeks. Scale bar, 50 μm. Immunofluorescence of keratin 14 and Ki67 expression. Scale bar, 50 μm. d, f Representative FACS plots showing the efficiency of bone marrow transplantation, activation of T cells, and intracellular expression of IL-17 and IL-22. Gating blood cells for CD45.1 and CD45.2 expression revealed more than 90% engraftment of donor cells in recipient mice. Lymphocytes were isolated from draining lymph nodes and stained for CD45.1, CD45.2, CD4, CD44, CD62L, CD122, IL-17, and IL-22, followed by flow cytometry.

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