Pathogenic mechanisms involved in psoriasiform skin lesions during anti-TNF-α therapy. Pathogenic mechanisms involved in psoriasiform skin lesions during anti-TNF-α therapy. TNF-α, IL-17 and IFN-α are the main cytokines that contribute to the development of psoriatic lesions. TNF-α inhibits the activity of plasmacytoid dendritic cells (pDC), which are key producers of IFN-α. During anti-TNF-α treatment, there is an unopposed IFN-α production by pDC. In parallel, IFN-α leads to the expression of chemokines such as CXCR3 on T cells, favouring T cell homing to the skin. IFN-α also stimulates and activates T cells to produce TNF-α and IL-17, sustaining inflammatory mechanisms for psoriasis lesions. IFN-α, interferon α; IL-17, interleukin 17; TNF-α, tumour necrosis factor α. Éric Toussirot, and François Aubin RMD Open 2016;2:e000239 Copyright © BMJ Publishing Group & EULAR. All rights reserved.