Keratinocytes derived from late-onset-psoriasis skin do not impair Langerhans cell migration

Chronic plaque psoriasis (CPP) is associated with over-expression of interleukin (IL)-17 and systemic antibody therapies targeting this cytokine are highly efficacious1 . Psoriasis presents as either early- or late-onset disease (before or after 40 years of age, respectively). Langerhans cells (LC) are the dendritic cells of the epidermis that regulate cutaneous immune responses2 . In the uninvolved skin of early-onset CPP there is impaired LC migration after exposure to a contact allergen, tumour necrosis factor-α (TNF-α) or IL-1β in vivo3 . However, in late-onset psoriasis there is impaired migration in response to TNF-α, but normal responses to IL-1β4 . We have recently shown that in early-onset psoriasis, LC migration is impaired as a result of IL-17A causing changes in the psoriasis keratinocyte secretome5 . Here we sought to examine whether keratinocytes isolated from uninvolved late-onset psoriasis skin also impair LC migration. This article is protected by copyright. All rights reserved.