Biological effects of IL-26 on T cell-mediated skin inflammation including psoriasis.
2019
Psoriasisis a chronic inflammatory skin disease characterized mainly by
epidermal hyperplasia, scaling, and
erythema;
T helper 17 cellshave a role in its pathogenesis. Although IL-26, known as a T helper 17 cytokine, is upregulated in psoriatic skin lesions, its precise role is unclear. We investigated the role of IL-26 in the
imiquimod-induced
psoriasis-like murine model using human IL-26 transgenic mice.
Erythemasymptoms induced by daily applications of
imiquimodincreased dramatically in human IL-26 transgenic mice compared with controls. Vascularization and immune cell infiltration were prominent in skin lesions of human IL-26 transgenic mice. Levels of fibroblast growth factor (FGF) 1, FGF2, and FGF7 were significantly upregulated in the skin lesions of
imiquimod-treated human IL-26 transgenic mice and
psoriasispatients. In vitro analysis demonstrated that
FGF1, FGF2, and FGF7 levels were elevated in human keratinocytes and vascular endothelial cells following IL-26 stimulation. Furthermore, IL-26 acted directly on vascular endothelial cells, promoting proliferation and tube formation, possibly through
protein kinase B, extracellular signal–regulated kinase, and NF-κB pathways. Moreover, similar effects of IL-26 were observed in the murine contact hypersensitivity model, indicating that these effects are not restricted to
psoriasis. Altogether, our data indicate that IL-26 may be a promising therapeutic target in T cell–mediated skin inflammation, including
psoriasis.
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