Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases

Research output: Contribution to journalArticle

181 Citations (Scopus)

Abstract

Classic atopic dermatitis is complicated by asthma, allergic rhinitis, and food allergies, cumulatively referred to as atopic diseases. Recent discoveries of mutations in the filaggrin gene as predisposing factors for atopic diseases have refocused investigators' attention on epidermal barrier dysfunction as a causative mechanism. The skin's barrier function has three elements: the stratum corneum (air-liquid barrier), tight junctions (liquid-liquid barrier), and the Langerhans cell network (immunological barrier). Clarification of the molecular events underpinning epidermal barrier function and dysfunction should lead to a better understanding of the pathophysiological mechanisms of atopic diseases.

Original languageEnglish
Pages (from-to)440-447
Number of pages8
JournalJournal of Clinical Investigation
Volume122
Issue number2
DOIs
Publication statusPublished - 2012 Feb

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Skin
Langerhans Cells
Food Hypersensitivity
Tight Junctions
Atopic Dermatitis
Causality
Cornea
Asthma
Air
Research Personnel
Mutation
Genes
filaggrin
Allergic Rhinitis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Epidermal barrier dysfunction and cutaneous sensitization in atopic diseases. / Kubo, Akiharu; Nagao, Keisuke; Amagai, Masayuki.

In: Journal of Clinical Investigation, Vol. 122, No. 2, 02.2012, p. 440-447.

Research output: Contribution to journalArticle

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