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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: J Invest Dermatol. 2017 Mar 1;137(7):1474–1483. doi: 10.1016/j.jid.2017.02.972

Figure 3. Glucocorticoid biosynthesis and steroid responses are suppressed in psoriatic skin.

Figure 3

RNA-sequencing was performed on psoriatic (PP), uninvolved (PN) and normal (NN) skin (n=6) matching patients analyzed by metabolic profiling. (a) Glucocorticoid biosynthetic pathway. (b–c) Suppression of gene and protein expression involving key enzymes in the glucocorticoid biosynthetic pathway. (d) Reduced nuclear localization of the glucocorticoid receptor in psoriatic skin (scale bar = 100μm). (e) IL-17A and IL-22 at 10ng/ml suppressed HSD11B1 and HSD11B2 expression, whereas TNF-α (10ng/ml) had no effect in 3D epidermal raft cultures. Combination of IL-17A/IL-22 and TNF-α (cytomix) suppressed HSD11B1 and HSD11B2 expression, accompanied by decreased expression of desmoglein 1 (DSG1), filaggrin (FLG) and loricrin (LOR), but increased expression of IL36G and DEFB4. (Data shown with SEM, n=2–10, **p<0.01, ***p<0.001, for IHC and IF representative figures are shown (n=3)).