Fig. 3.

Inflammation in IMQ-induced dermatitis. (A) Increase in skinfold thickness, measured as the difference between skin fold thickness on day 0 and day 6 (n = 7–8). (B) Representative H&E staining of untreated (Left, control) or IMQ-treated (Middle and Right, IMQ) skin from mice of the indicated genotypes. a, acanthosis; d, dermal infiltration; pu, pustule. The right panel shows higher-power magnifications of the inset in the middle panel, demonstrating more infiltrating cells in the WT compared with the TTPΔARE section. (C) Shown are Ly6G immunostained sections from control (Left) and IMQ-treated (Right) mice of the indicated genotypes (n = 4–5). (D) Ly6G positive cells in Fig. 4C were quantitated as the number of cells in one high-power field (400×) in an area of maximal infiltration from each animal (n = 4–5). (E) Histopathology scores were determined for five lesions, namely, epidermal hyperplasia, hyperkeratosis, parakeratosis, parakeratotic inflammation, and dermal inflammation. Severity was graded on a four-point scale. Each mean score is depicted by a black line and each point represents data from one animal (n = 7–8). (F) NanoString gene expression analysis was performed on RNA isolated from affected skin. Shown are the normalized counts for the 11 transcripts that were significantly down-regulated in the TTPΔARE group compared with the WT group (n = 6). Statistical analysis was performed by two-tailed unpaired Student’s t test for A, D, E, and F. Error bars represent SEM; *P < 0.05, **P < 0.01.