Genetic variations in the proinflammatory cytokine IL-23 are associated with psoriasis, a common, inflammatory skin disorder (Nair et al., 2009). IL-23 is primarily produced by dendritic cells (DCs) and plays a pathogenic role in psoriasis by directing the development of T helper type 17 cells (Di Cesare et al., 2009). Langerhans cells (LCs), the main DC subtype in the epidermis, can participate in both immunity and the induction of tolerance (Igyarto et al., 2011, Seneschal et al., 2012), yet their role in psoriasis remains unclear. Mouse models of disease have yielded contradictory results (Glitzner et al., 2014, Wohn et al., 2013, Yoshiki et al., 2014). However, the migration of LCs is impaired in human disease, and it was suggested that the inflammatory environment of psoriasis may affect their function (Cumberbatch et al., 2006). This study sought to clarify the role of LC role in disease with specific focus on the production of IL-23.

Punch biopsies (6 mm) were obtained from psoriasis patients and healthy controls after written informed patient consent and ethical approval were obtained from St. Vincent’s Ethics and Medical Research Committee. LCs in epidermal suspensions were identified as live single CD45+ CD1a+ CD207+ cells (Figure 1 a; see Supplementary Materials online). A significantly higher percentage of epidermal LCs expressed IL-23p19 or coexpressed p40 and p19 in psoriatic lesional and perilesional biopsies compared with LCs from healthy epidermis (P< 0.01, P< 0.05; Figure 1 a). There was no significant difference in the expression of IL-12p40 only (Figure 1 a). These results suggest that under inflammatory conditions, LCs are capable of producing proinflammatory cytokines that promote T helper type 17 cell development.