Atopic dermatitis (AD) is a common disease, with an increasing prevalence. The primary pathogenesis of the disease is still elusive, resulting in lack of specific treatments. It is known that Th2 predominate in acute AD, and a switch to Th1 is characteristic of chronic disease. The objective of the study is to identify factors that participate in the onset of lesions and maintenance of chronic lesions.

Acute, chronic, and non-lesional skin samples were collected from ten patients with moderate-to-severe AD that met our inclusion criteria, under an institutional review board–approved protocol. The following criteria were employed to define acute AD and distinguish true acute from “acute on chronic” skin lesions: a) new lesions of <72 hours duration, as previously defined;14 b) lack of skin lichenification; c) lack of regenerative hyperplasia, as defined by epidermal thickness ?150? [hematoxylin and eosin (H&E)] and basal or confluent supra-basal Keratin 16 (K16) positivity. No systemic or topical treatments were allowed for ?4 weeks prior to biopsies. Biopsy specimens were frozen in optimal cutting temperature (OCT) for immunohistochemistry (IHC) and liquid nitrogen for RNA extraction.

Progression of skin lesions.

non-lesional skin biopsies from 10 atopic dermatitis patients.

Biopsy specimens were frozen in optimal cutting temperature (OCT) for immunohistochemistry (IHC) and liquid nitrogen for RNA extraction.