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- W4366181251 abstract "IL-36 cytokine family, belonging to IL-1 cytokine family, includes three agonists, IL-36α, IL-36β, and IL-36γ and one antagonist, IL-36 receptor antagonist, all of which bind to IL-36 receptor. Various types of cells in skin, including epidermal keratinocytes, dermal fibroblasts and endothelial cells, as well as several immune cells produce IL-36 cytokines and Th17 cytokines are associated with the production. IL-36 cytokines have the capacity to augment Th17 immune responses by activation of plasmacytoid dendritic cells and induction of CCL20 from epidermal keratinocytes. They also induce CXCL1, CXCL2, and CXCL8 induction from epidermal keratinocytes, resulting in neutrophil infiltration in the skin. Although Th17 immune response involvement in atopic dermatitis (AD) is still under debate, increased IL-36α and IL-36γ expression was reported in AD and the efficacy of IL-36 receptor antibody, spesolimab, in AD was demonstrated recently in one clinical study. In this study, we examined the expression and involvement of IL-36β in AD. Serum IL-36β levels were increased in AD patients compared to healthy controls, whereas the levels were not correlated with clinical and laboratory disease severity markers. We next examined IL-36β effect on epidermal keratinocytes using HaCaT cells. IL-36β upregulated both mRNA and protein of vascular endothelial growth factor (VEGF) from HaCaT cells in a dose-dependent manner. The inhibitor of the ERK1/2 pathway but not p38 MAPK, Akt, and NF-κB pathways dampened the IL-36β-induced VEGF expression from HaCaT cells. Collectively, IL-36β may contribute to angiogenesis in AD through VEGF expression from epidermal keratinocytes." @default.
- W4366181251 created "2023-04-19" @default.
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- W4366181251 date "2023-05-01" @default.
- W4366181251 modified "2023-09-28" @default.
- W4366181251 title "1574 Increased IL-36β may contribute to angiogenesis though vascular endothelial growth factor induction from epidermal keratinocytes in atopic dermatitis" @default.
- W4366181251 doi "https://doi.org/10.1016/j.jid.2023.03.1592" @default.
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