Abstract

Psoriasis is a common chronic inflammatory skin disease characterized by abnormal proliferation/differentiation of keratinocytes (KCs) and increased immune cell infiltration in the dermis and epidermis (Greb et al., 2016). Although immune cells are considered to be the main driver of psoriasis, KCs may also be implicated in triggering psoriasis and in sustaining inflammation in psoriatic skin (Ni and Lai, 2020). Psoriasis can manifest clinically in several different ways (Boehncke and Schön, 2015), but the rare observation that some individuals may present with psoriasis along the lines of Blaschko (Blaschko, 1901), that is, in a distribution fitting lines of epidermal development and therefore inherent KC pathology (Happle, 1993), provides an opportunity to dissect KC pathobiology in psoriasis in more detail.

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