Molecular mechanisms of cutaneous inflammatory disorder: Atopic dermatitis

Jung Eun Kim, Jong Sic Kim, Dae Ho Cho, Hyun Jeong Park

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

Atopic dermatitis (AD) is a multifactorial inflammatory skin disease resulting from interactions between genetic susceptibility and environmental factors. The pathogenesis of AD is poorly understood, and the treatment of recalcitrant AD is still challenging. There is accumulating evidence for new gene polymorphisms related to the epidermal barrier function and innate and adaptive immunity in patients with AD. Newly-found T cells and dendritic cell subsets, cytokines, chemokines and signaling pathways have extended our understanding of the molecular pathomechanism underlying AD. Genetic changes caused by environmental factors have been shown to contribute to the pathogenesis of AD. We herein present a review of the genetics, epigenetics, barrier dysfunction and immunological abnormalities in AD with a focus on updated molecular biology.

Original languageEnglish
Article number1234
JournalInternational journal of molecular sciences
Volume17
Issue number8
DOIs
Publication statusPublished - 2016 Aug 1
Externally publishedYes

Fingerprint

dermatitis
Atopic Dermatitis
disorders
Skin
pathogenesis
molecular biology
Molecular biology
T-cells
polymorphism
abnormalities
immunity
Adaptive Immunity
Genetic Predisposition to Disease
Polymorphism
Chemokines
Skin Diseases
Innate Immunity
Epigenomics
genes
Dendritic Cells

Keywords

  • Atopic dermatitis
  • Barrier
  • Epigenomics
  • Genetics
  • Immunologic abnormalities

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Molecular mechanisms of cutaneous inflammatory disorder : Atopic dermatitis. / Kim, Jung Eun; Kim, Jong Sic; Cho, Dae Ho; Park, Hyun Jeong.

In: International journal of molecular sciences, Vol. 17, No. 8, 1234, 01.08.2016.

Research output: Contribution to journalReview article

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