IL-33 is secreted by psoriatic keratinocytes and induces pro-inflammatory cytokines via keratinocyte and mast cell activation

• Published in: Experimental dermatology 2012-11, Vol.21 (11), p.892-894
• Main Authors: Balato, Anna, Lembo, Serena, Mattii, Martina, Schiattarella, Maria, Marino, Rita, De Paulis, Amato, Balato, Nicola, Ayala, Fabio
• Format: Article
• Language: English
• Subjects: Adult; Arthritis; Biological and medical sciences; Cell Line; Cells, Cultured; Chemokine CCL2 - metabolism; Cytokines - metabolism; Dermatology; Humans; IL-33; In Vitro Techniques; Interleukin-33; Interleukin-6 - metabolism; Interleukins - metabolism; Interleukins - pharmacology; Keratinocytes - drug effects; Keratinocytes - metabolism; Keratinocytes - pathology; Mast Cells - pathology; Medical sciences; psoriasis; Psoriasis - metabolism; Psoriasis - pathology; Psoriasis. Parapsoriasis. Lichen; Tumor Necrosis Factor-alpha - pharmacology; Vascular Endothelial Growth Factor A
• ISSN: 0906-6705; 1600-0625
• DOI: 10.1111/exd.12027

IL‐33 is a novel pro‐inflammatory cytokine and ligand for the orphan receptor ST2. Although originally defined as an inducer of Th2‐mediated responses, IL‐33 was recently found to be involved in arthritis, a Th1/Th17‐mediated disease. Here, we assessed the ability of IL‐33 to promote inflammation via mast cells (MCs) and keratinocytes (KCs) activation in psoriasis. IL‐33 resulted elevated in the skin but not in the serum of psoriasis patients. IL‐33 was secreted by psoriasis KCs and HaCaT cells after TNF‐α stimulation. In HMC‐1, TNF‐α, but not IL‐17, could induce a robust increase in IL‐33 expression. In HaCaT cells, TNF‐α was able to induce IL‐6, MCP‐1 and VEGF, and the addition of IL‐33 reinforced these increases. TNF‐α + IL‐33 combination showed similar results in primary KCs and ex vivo skin organ culture. In conclusion, our study suggests that IL‐33 may be involved in psoriasis biology via MCs and KCs.