Immune-mediated Skin Inflammation is Similar in Severe Atopic Dermatitis Patients With or Without Filaggrin Mutation

Inflammatory cytokines can impair the skin barrier,but the question as to whether barrier alterations affectkeratinocyte immune responses remains unanswered.The aim of this study was to investigate whetherimmune-mediated skin inflammation differs between severeatopic dermatitis patients with or without filaggrinmutation. The levels of filaggrin, inflammatory T helper2 polarizing cytokines (thymic stromal lymphopoietin(TSLP) and interleukin 33 (IL-33)) and chemokine (C-Cmotif) ligand 27 (CCL27), histological severity markers,T-cell and dendritic cell counts in biopsies from lesionalskin of severe atopic dermatitis patients with and withoutfilaggrin mutation and healthy skin were quantifiedby immunohistochemistry. The results were confirmedby quantitative PCR analyses. No significant differenceswere found between the 2 patient groups. Expression ofatopic dermatitis-specific cytokines showed significantcorrelation with histological severity. These findingssuggest that the immune-mediated skin inflammation(represented by keratinocyte-derived factors, T-cell anddendritic cell counts) is similar in the 2 patient groupswith severe atopic dermatitis, and that immune activationis connected to the severity of the disease ratherthan to the origin of barrier alterations. Key words:atopic dermatitis; filaggrin; immunohistochemistry; innateimmunity; thymic stromal lymphopoietin.Accepted Oct 29, 2015; Epub ahead of print Nov 5, 201