Fig. 3: IL-38 inhibits IL-36γ-induced P38 and NF-κB signalings, as well as regulates the expression of differentiation markers and inflammatory molecules in human keratinocytes. | Cell Death & Disease

Fig. 3: IL-38 inhibits IL-36γ-induced P38 and NF-κB signalings, as well as regulates the expression of differentiation markers and inflammatory molecules in human keratinocytes.

From: IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment

Fig. 3

All experiments were performed on keratinocyte cultures (n = 3 strains) undergoing terminal differentiation and stimulated or not with IL-36γ in presence or absence of the indicated doses of IL-38 or IL-36Ra. a Protein extracts were obtained from keratinocyte cultures stimulated for 24 h and subjected to WB analysis to detect P38 and P65 phosphorylation. Filters were probed with anti-P38 and -P65 Abs. b Keratinocyte cultures were analyzed for KRT1, KRT10, Loricrin and ΔNp63 expression by WB. a, b β-actin was used as loading control and DI ratio indicates the densitometric intensity of the indicated phosphorylated/unphosphorylated proteins shown in one representative of three different WB. c mRNA levels of CXCL8, CCL20, VEGF-A, IL-6, HBD-2, and LL-37 were detected by real-time PCR analysis in keratinocytes stimulated for 6 h and normalized for GAPDH mRNA levels. TNF-α treatment was used as positive control. d ICAM-1 expression was evaluated by flow cytometry analysis on keratinocytes stimulated for 24 h with IL-36γ (50 ng/ml) and shown as mean fluorescence intensity. All data shown are the mean of three different experiments. c *p ≤ 0.05 and p** ≤ 0.01 compared with untreated or IL-36γ-treated cultures, as assessed by Mann–Whitney U test

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