Journal
EXPERIMENTAL DERMATOLOGY
Volume 26, Issue 5, Pages 402-408Publisher
WILEY
DOI: 10.1111/exd.13228
Keywords
endothelial; IL-36; inflammation; psoriasis; skin
Categories
Funding
- Faculty of Life Sciences
- University of Bradford
- MRC [MR/M01942X/1]
- BSF [BSF 5035]
- MRC [MR/M01942X/1, MR/L008505/1] Funding Source: UKRI
- British Skin Foundation [5035s] Funding Source: researchfish
- Medical Research Council [MR/L008505/1, MR/M01942X/1] Funding Source: researchfish
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Interleukin-36 cytokines are predominantly expressed by epithelial cells. Significant upregulation of epidermal IL-36 is now a recognised characteristic of psoriatic skin inflammation. IL-36 is known to induce inflammatory responses in dendritic cells, fibroblasts and epithelial cells. Although vascular alterations are a hallmark of psoriatic lesions and dermal endothelial cells are well known to play a critical role in skin inflammation, the effects of IL-36 on endothelial cells are unexplored. We here show that endothelial cells including dermal microvascular cells express a functionally active IL-36 receptor. Adhesion molecules VCAM-1 and ICAM-1 are upregulated by IL-36 stimulation, and this is reversed by the presence of the endogenous IL-36 receptor antagonist. IL-36-stimulated endothelial cells secrete the proinflammatory chemokines IL-8, CCL2 and CCL20. Chemotaxis assays showed increased migration of T-cells following IL-36 stimulation of endothelial cells. These results suggest a role for IL-36 in the dermal vascular compartment, and it is likely to enhance psoriatic skin inflammation by activating endothelial cells and promoting leucocyte recruitment.
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