Fig. 4: Peli1 induces the development of psoriasis-like disease via a Th17 cell response.

a Adult rtTA control mice and rtTA-Peli1 inducible transgenic mice were treated with doxycycline (2 mg/mL) for 12 and 24 weeks. Quantification of CD3⁺ cells and CD31⁺ vessels based on five skin sections obtained from five independent mice with the indicated genotypes (n = 3 mice per genotype). b Flow cytometry of T cells derived from rtTA and rtTA-Peli1 mice following treatment with doxycycline for 24 weeks. Immunocytes were isolated from the draining lymph nodes (inguinal, axillary, brachial, and cervical lymph nodes) of rtTA and rtTA-Peli1 mice. Cells were stained with CD3, CD4, CD44, CD62L, and CD122, followed by flow cytometry. Gated CD3⁺CD4⁺ T cells were analyzed for CD62L, CD44, and CD122 expression. c Heat map depicting real-time quantitative PCR (qRT-PCR) analysis of inflammation-related genes in skin samples obtained from doxycycline-treated rtTA and rtTA-Peli1 mice (two representing each genotype). Genes were ranked based on fold change in expression. The expression of genes above the dashed line was highly elevated in lesional skin samples derived from mice overexpressing Peli1 (rtTA-Peli1 mice with doxycycline treatment). d Comparison of Th17-related cytokine levels in doxycycline-treated rtTA and rtTA-Peli1 mice. Quantitative RT-PCR for cytokine expression was performed using skin tissues. Data are presented as the means ± SEMs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001; ns not significant; two-way ANOVA.