Immune-mediated skin inflammation is similar in severe atopic dermatitis patients with or without filaggrin mutation

Zsolt Dajnoki, Gabriella Béke, Gábor Mócsai, Anikó Kapitány, Krisztián Gáspár, Krisztina Hajdu, Gabriella Emri, Bence Nagy, Ilona Kovács, Lívia Beke, Balázs Dezső, Andrea Szegedi

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Inflammatory cytokines can impair the skin barrier, but the question as to whether barrier alterations affect keratinocyte immune responses remains unanswered. The aim of this study was to investigate whether immune-mediated skin inflammation differs between severe atopic dermatitis patients with or without filaggrin mutation. The levels of filaggrin, inflammatory T helper 2 polarizing cytokines (thymic stromal lymphopoietin (TSLP) and interleukin 33 (IL-33)) and chemokine (C-C motif) ligand 27 (CCL27), histological severity markers, T-cell and dendritic cell counts in biopsies from lesional skin of severe atopic dermatitis patients with and without filaggrin mutation and healthy skin were quantified by immunohistochemistry. The results were confirmed by quantitative PCR analyses. No significant differences were found between the 2 patient groups. Expression of atopic dermatitis-specific cytokines showed significant correlation with histological severity. These findings suggest that the immune-mediated skin inflammation (represented by keratinocyte-derived factors, T-cell and dendritic cell counts) is similar in the 2 patient groups with severe atopic dermatitis, and that immune activation is connected to the severity of the disease rather than to the origin of barrier alterations.

Original languageEnglish
Pages (from-to)645-650
Number of pages6
JournalActa Dermato-Venereologica
Volume96
Issue number5
DOIs
Publication statusPublished - Jan 1 2016

    Fingerprint

Keywords

  • Atopic dermatitis
  • Filaggrin
  • Immunohistochemistry
  • Innate immunity
  • Thymic stromal lymphopoietin

ASJC Scopus subject areas

  • Dermatology

Cite this