The role of T cells and interleukin‐17A in Behçet disease

Abstract

British Journal of DermatologyVolume 185, Issue 6 p. e201-e201 Plain Language Summary The role of T cells and interleukin-17A in Behçet disease First published: 17 December 2021 https://doi.org/10.1111/bjd.20788AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract Linked Article: Vural et al. Br J Dermatol 2021; 185:1209–1220. Behçet disease (BD) is a severe chronic inflammatory disease. It damages blood vessels and can affect all organs, including the skin, eyes and brain. This can lead to blindness or even death. BD is common along the historical ‘Silk Road’, extending from Europe to the Far East, especially in Turkey. To find out what causes the disease, researchers from Turkey, Germany and Japan investigated skin lesions from patients with BD. BD is associated with the genes for HLA-B*51, ERAP1 and the interleukin (IL)-23 receptor. These genes determine targets of CD8+ T-cell responses and the production of the immune mediator IL-17. High levels of IL-17 in the blood are characteristic of BD. In psoriasis, another inflammatory skin disease, an HLA-class I molecule, together with ERAP1, induces an autoimmune response (where the body’s immune system attacks its own healthy cells and tissues) and high IL-17 production by CD8+ T cells against the pigment-producing cells of the skin, the melanocytes. This suggests a similar autoimmune disease pathway in BD. We found that in skin lesions from patients with BD activated CD8+ T cells producing high levels of IL-17 induced by IL-23 prefer to accumulate around blood vessels. This causes recruitment and activation of neutrophilic granulocytes, which contribute to tissue damage by forming networks of released DNA. These findings propose that in BD dysregulated CD8+ T cells wrongly attack the body’s own blood vessels. This study improves our understanding of how these genetic traits contribute to a disease pathway, which may help to develop new and effective treatments for BD targeting IL-17 or IL-23. Volume185, Issue6December 2021Pages e201-e201 RelatedInformation