IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation.

Senra, Luisa; Mylonas, Alessio; Kavanagh, Ruairi D; Fallon, Padraic G; Conrad, Curdin; Borowczyk-Michalowska, Julia; Wrobel, Ludovic Jean; Kaya, Guerkan; Yawalkar, Nikhil; Boehncke, Wolf-Henning; Brembilla, Nicolo Costantino (2019). IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation. Journal of investigative dermatology, 139(8), 1732-1742.e17. Elsevier 10.1016/j.jid.2019.01.021

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IL-17E (IL-25) is a member of the IL-17 cytokine family involved in the promotion of type 2 immune responses. Recently, IL-17E has been reported to be up-regulated in distinct skin inflammatory diseases such as psoriasis and atopic and contact dermatitis. We assessed the role played by IL-17E in skin inflammation. Here, we show that IL-17E induces skin inflammation in vivo, characterized by the expression of innate immune response genes and the recruitment of innate immune cells, particularly neutrophils. Genetic deletion or IL-17E neutralization ameliorated skin inflammation induced by imiquimod application or tape stripping, with reductions in neutrophil and macrophage infiltration as assessed by t-distributed stochastic neighbor embedding-guided multiparameter flow cytometry analysis, in mice. In humans, IL-17E promotes the recruitment of neutrophils via activation of macrophages in a p38-dependent mechanism. In addition, IL-17E is up-regulated in neutrophil-rich inflammatory skin diseases, such as pyoderma gangrenosum and acute generalized exanthematous pustulosis. Our data show a role for IL-17E in skin inflammation that is unrelated to the development of type 2 immune reactions. We propose that IL-17E is an important common denominator of chronic skin inflammation, promoting innate immune cell recruitment and activation.

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