Additional file 1 of Genetic deletion of microsomal prostaglandin E synthase-1 promotes imiquimod-induced psoriasis in mice

Supplementary Material 1. Figure S1. In vivo depletion of γδ T cells by anti-TCRγδ polyclonal antibody. Schematic representation of the experimental plan. Solid allows indicate timepointat which the intraperitoneal injection of the antibody were performed. The efficacy of γδ T-cell depletion was confirmed through an FCM analysis of the skin samples. The administration of anti-TCRγδ antibody was successful in maintaining a significant decrease in the TCRγδ-positive γδ T cells but not TCRβ-positive αβ T cells for 7 days after the antibody administration. Figure S2. In vivo depletion of CD4-positive T cells by anti-CD4 monoclonal antibody. Schematic representation of the experimental plan. Solid allows indicate time-pointat which intraperitoneal injection of the antibody were performed. The efficacy of CD4-positive T cell depletion was confirmed by FCM analysis of T cell population in the peripheral bloodand spleen. FCM analysis confirmed that anti-CD4 antibody treatment effectively reduced the number of CD3+ CD4+ T cells but not CD3+ CD8+ T cells in the peripheral blood and spleen of the treated mice compared to the control mice. *P < 0.05 vs. control; t-test. Figure S3. Effect of pharmacological DP receptor inhibition on facilitated psoriasis under the condition of mPGES-1 deficiency. Given that PGD2 production was increased in the skin of mPGES-1−/− mice after the induction of psoriasis, we investigated the effects of PGD2 in the IMQ-induced psoriasis pathology under the condition of mPGES-1 deficiency using antagonists specific for each DP subtype DP1 and DP2. DP1 antagonist BWA868C was administered intraperitoneally to the mPGES-1−/− mice at a dose of 1 mg/kg daily for 6 days immediately before the IMQ treatment, and the psoriasis pathology was evaluated. There was no significant difference in the skin scaling and thickening scores between mPGES-1−/− mice treated with a DP1 antagonist and mPGES-1−/− mice treated with a vehicle. The DP2 antagonist CAY10471 was administered intraperitoneally to the mPGES-1−/− mice at a dose of 2 mg/kg daily for 6 days immediately before the IMQ treatment. Similarly, there was no significant difference in both scores between the DP2 antagonist and vehicle control in mPGES-1−/− mice. These results suggest that PGD2, which is increased in the skin of psoriasis-induced mPGES-1−/− mice, is unlikely to exacerbate or alleviate the major symptoms of IMQ-induced psoriasis. *P < 0.05; ANOVA followed by Tukey’s multiple comparison test.