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IL ‐33 is secreted by psoriatic keratinocytes and induces pro‐inflammatory cytokines via keratinocyte and mast cell activation
Author(s) -
Balato Anna,
Lembo Serena,
Mattii Martina,
Schiattarella Maria,
Marino Rita,
Paulis Amato,
Balato Nicola,
Ayala Fabio
Publication year - 2012
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12027
Subject(s) - hacat , psoriasis , keratinocyte , immunology , interleukin 33 , mast cell , tumor necrosis factor alpha , inflammation , cytokine , orphan receptor , medicine , interleukin , biology , cell culture , genetics , gene , transcription factor , biochemistry
IL ‐33 is a novel pro‐inflammatory cytokine and ligand for the orphan receptor ST 2. Although originally defined as an inducer of T h2‐mediated responses, IL ‐33 was recently found to be involved in arthritis, a T h1/ T h17‐mediated disease. Here, we assessed the ability of IL ‐33 to promote inflammation via mast cells (MCs) and keratinocytes ( KC s) activation in psoriasis. IL ‐33 resulted elevated in the skin but not in the serum of psoriasis patients. IL ‐33 was secreted by psoriasis KC s and H a C a T cells after TNF ‐α stimulation. In HMC ‐1, TNF ‐α, but not IL ‐17, could induce a robust increase in IL ‐33 expression. In H a C a T 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 KC s and ex vivo skin organ culture. In conclusion, our study suggests that IL ‐33 may be involved in psoriasis biology via MCs and KC s.