Figure 7
From: Small Molecule IL-36γ Antagonist as a Novel Therapeutic Approach for Plaque Psoriasis
A-552 attenuates hIL-36γ induced inflammation in human 3D skin equivalents. (A) Staining of fully differentiated 3D skin equivalents untreated or treated with 0.3 μg/mL hIL-36γ alone or in the presence of function blocking 10 μg/mL anti-hIL-36R or 10 μM A-552. Representative images at 32X magnification are shown. (B) Differences between RNA transcript levels in treated and non-treated 3D skin equivalents were quantified for each probe using qRT-PCR. Average of 6 treated and 7 control samples is shown ± S.E.M. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 using ANOVA with Dunnett’s post hoc test vs. hIL-36γ alone; (F; DF) = 26.05; 24 (S100A7), 75.76; 24 (DEFB4), 82.13; 24 (Elafin), 6.221; 24 (K16), 19.53; 23 (Involucrin), 13.16; 24 (K10)). (C) Differences between secreted CXCL1, IL-8 and IL-6 proteins in treated and non-treated 3D skin equivalents were quantified using immunoassays. Average of 6 treated (5 in CXCL1 and IL-8 NT column) and 7 control samples is shown ± S.E.M. (**p < 0.01, ****p < 0.0001 using ANOVA with Dunnett’s post hoc test vs. hIL-36γ alone; (F; DF) = 61.15; 23 (CXCL1), 21.31; 23 (IL-8), 32.46; 24 (IL-6)).
