| First Author | Senra L | Year | 2019 |
| Journal | J Invest Dermatol | Volume | 139 |
| Issue | 8 | Pages | 1732-1742.e17 |
| PubMed ID | 30738055 | Mgi Jnum | J:284093 |
| Mgi Id | MGI:6388642 | Doi | 10.1016/j.jid.2019.01.021 |
| Citation | Senra L, et al. (2019) IL-17E (IL-25) Enhances Innate Immune Responses during Skin Inflammation. J Invest Dermatol 139(8):1732-1742.e17 |
| abstractText | 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. |
