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Int. J. Mol. Sci. 2016, 17(8), 1234; doi:10.3390/ijms17081234

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

1
Department of Dermatology, St. Paul’s Hospital, College of Medicine, The Catholic University of Korea, Seoul 02559, Korea
2
Department of Dermatology, Yeouido St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, 62 Yeouido-dong, Yeongdeungpo-gu, Seoul 07345, Korea
3
Department of Life Science, SookmyungWomen’s University, Seoul 140-742, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Chris Jackson
Received: 31 May 2016 / Revised: 21 July 2016 / Accepted: 26 July 2016 / Published: 30 July 2016
(This article belongs to the Special Issue Inflammatory Skin Conditions)
View Full-Text   |   Download PDF [797 KB, uploaded 30 July 2016]   |  

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. View Full-Text
Keywords: atopic dermatitis; genetics; epigenomics; barrier; immunologic abnormalities atopic dermatitis; genetics; epigenomics; barrier; immunologic abnormalities
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Kim, J.E.; Kim, J.S.; Cho, D.H.; Park, H.J. Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis. Int. J. Mol. Sci. 2016, 17, 1234.

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