Fig. 1: Correlation between Peli1 expression and the development of psoriasis-like skin inflammatory disease.

a Psoriasis-like skin inflammation was induced by topical application of imiquimod (IMQ) cream daily for six consecutive days. Control (Cont) indicates equivalent volume of Vaseline treatment. b To induce atopic dermatitis-like symptoms, dinitrochlorobenzene (DNCB) was topically applied to BALB/c mice. One day after dorsal hair removal, 1% DNCB was applied. Five days after dorsal hair removal, 0.2% DNCB was applied as described in the “Materials and methods” section. c Psoriasis-like skin generated by IMQ cream. H&E-stained sections of skin (top) and immunohistochemistry of Peli1 (middle) and Psoriasin (bottom) encoded by the S100A7 gene overexpressed in psoriasis. Scale bars, 50 μm. d Atopic dermatitis-like skin generated by DNCB application. H&E-stained sections of skin (top) and immunohistochemistry of Peli1 (middle) and Periostin (bottom) encoded by the S100A7 gene with overexpression in psoriasis. Scale bars, 50 μm. e Comparison of Peli1 mRNA levels in healthy human skin (n = 64) and nonlesional skin (n = 58) and lesional skin (n = 58) samples of psoriasis patients. Microarray data sets processed with the robust multichip average (RMA) method were retrieved from the Gene Expression Omnibus (GEO) Database (accession number: GSE 13355). Expression values in the dot graph are adjusted for RMA expression values (log scale) to account for batch and sex effects. Data are presented as the means ± SEMs. *P < 0.05, **P < 0.01, ***P < 0.001; ns not significant based on Student’s t-test. f Normal human skin (breast) immunostained for Peli1 (left 40×). Psoriasis lesion immunostained for Peli1 (right, 40×). Scale bars, 50 μm. g Peli1 expression was evaluated semiquantitatively by comparing the intensity of expression between healthy skin (H) and psoriatic skin lesions (P) in the spinous layer and infiltrated immune cells.