Skin samples from children and adult patients with AD share lipid metabolism and tight junction alterations, but epidermal differentiation complex defects are only present in adult AD, potentially resulting from chronic immune aberration that is not yet present in early-onset disease.

We recommend using these strata for interpretation of their respective measures in clinical trials of AD. There are important differences between the five assessments, which profoundly impact the interpretation of their scores.

The skin phenotype of new-onset pediatric AD is substantially different from that of adult AD. Although excess T2 activation characterizes both, T9 and T17 are highly activated at disease initiation. Increases in IL-19 levels might link T2 and T17 activation.

Bullous pemphigoid (BP) is an autoimmune blistering skin disease caused by autoantibody against the hemidesmosomal protein BP180. B regulatory cells (Bregs) are crucial in maintaining self-tolerance and suppressing autoantibody production. Blood samples were collected from thirty-six BP patients and thirty healthy volunteers. The number of CD19 + CD24 hi CD27 + Bregs was analyzed by flow cytometry. Elisa assay was performed to detect the level of anti-BP180 autoantibodies produced by patient-derived peripheral blood mononuclear cells (PBMCs) with Bregs deletion or without. In addition, T cells were cultured with autogenous Bregs from BP patients or healthy controls respectively, then the proliferation and cytokine productions in these T cells were detected by flow cytometry. Finally, the expressions of IL-10 and TNF-a in Bregs were further examined. Then etanercept was added into the culture of patients-derived PBMCs to investigate the role of TNF-a in autoantibody production. The frequency of circulating CD19 + CD24 hi CD27 + Bregs increased in BP patients compared with healthy controls. However, patient-derived Bregs were impaired in suppressing the production of specific anti-BP180 autoantibodies. These patients-derived Bregs were also defective in suppressing CD4 + T cell activation. Further, patient-derived Bregs produced comparable level of IL-10, while aberrantly secreted TNF-a. Etanercept could inhibit the autoantibody production in patient-derived PBMCs. Our results suggested that BP patient-derived Bregs were impaired in suppressing CD4 + T cell activation in a manner of aberrant secretion of TNF-a, rather than IL-10, thus contributing to the autoantibody production.

Skin pain is a common and burdensome symptom in AD. Skin pain severity should be assessed with itch severity in AD patients and may be an important end point for monitoring treatment response.