View/ Open
Main article (1.024Mb)
Download
Publication date
2017-02Rights
© 2017 Wiley This is the peer reviewed version of the following article: Bridgewood C, Stacey M, Alase A, Lagos D, Graham A and Wittmann M (2016) IL-36γ has proinflammatory effects on human endothelial cells. Experimental Dermatology. 26(5): 402-408, which has been published in final form at https://doi.org/10.1111/exd.13228. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.Peer-Reviewed
YesOpen Access status
openAccessAccepted for publication
2016-09-14
Metadata
Show full item recordAbstract
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-36γ stimulation and this is reversed by the presence of the endogenous IL-36 receptor antagonist. IL-36γ stimulated endothelial cells secrete the proinflammatory chemokines IL-8, CCL2 and CCL20. Chemotaxis assays showed increased migration of T cells following IL-36γ stimulation of endothelial cells. These results suggest a role for IL-36γ in the dermal vascular compartment and it is likely to enhance psoriatic skin inflammation by activating endothelial cells and promoting leukocyte recruitment.Version
Accepted manuscriptCitation
Bridgewood C, Stacey M, Alase A, Lagos D, Graham A and Wittmann M (2016) IL-36γ has proinflammatory effects on human endothelial cells. Experimental Dermatology. 26(5): 402-408.Link to Version of Record
https://doi.org/10.1111/exd.13228Type
Articleae974a485f413a2113503eed53cd6c53
https://doi.org/10.1111/exd.13228