| Nonlesional atopic dermatitis skin is characterized by broad terminal differentiation defects and variable immune abnormalities. | |
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MedLine Citation:
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PMID: 21388663 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Atopic dermatitis (AD) is a common inflammatory skin disease with a T(H)2 and "T22" immune polarity. Despite recent data showing a genetic predisposition to epidermal barrier defects in some patients, a fundamental debate still exists regarding the role of barrier abnormalities versus immune responses in initiating the disease. An extensive study of nonlesional AD (ANL) skin is necessary to explore whether there is an intrinsic predisposition to barrier abnormalities, background immune activation, or both in patients with AD. OBJECTIVE: We sought to characterize ANL skin by determining whether epidermal differentiation and immune abnormalities that characterize lesional AD (AL) skin are also reflected in ANL skin. METHODS: We performed genomic and histologic profiling of both ANL and AL skin lesions (n = 12 each) compared with normal human skin (n = 10). RESULTS: We found that ANL skin is clearly distinct from normal skin with respect to terminal differentiation and some immune abnormalities and that it has a cutaneous expansion of T cells. We also showed that ANL skin has a variable immune phenotype, which is largely determined by disease extent and severity. Whereas broad terminal differentiation abnormalities were largely similar between involved and uninvolved AD skin, perhaps accounting for the "background skin phenotype," increased expression of immune-related genes was among the most obvious differences between AL and ANL skin, potentially reflecting the "clinical disease phenotype." CONCLUSION: Our study implies that systemic immune activation might play a role in alteration of the normal epidermal phenotype, as suggested by the high correlation in expression of immune genes in ANL skin with the disease severity index. |
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Authors:
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Mayte Suárez-Fariñas; Suzanne J Tintle; Avner Shemer; Andrea Chiricozzi; Kristine Nograles; Irma Cardinale; Shenghui Duan; Anne M Bowcock; James G Krueger; Emma Guttman-Yassky |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: The Journal of allergy and clinical immunology Volume: 127 ISSN: 1097-6825 ISO Abbreviation: J. Allergy Clin. Immunol. Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-04-04 Completed Date: 2011-05-31 Revised Date: 2012-04-04 |
Medline Journal Info:
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Nlm Unique ID: 1275002 Medline TA: J Allergy Clin Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 954-64.e1-4 Citation Subset: AIM; IM |
Copyright Information:
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Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved. |
Affiliation:
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Laboratory for Investigative Dermatology, Rockefeller University, New York, NY 10065, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Aged Aged, 80 and over Cell Differentiation Dermatitis, Atopic / genetics, immunology*, pathology* Female Gene Expression Profiling* Humans Immunohistochemistry Keratinocytes / cytology Male Middle Aged Oligonucleotide Array Sequence Analysis Phenotype Reverse Transcriptase Polymerase Chain Reaction Young Adult |
| Grant Support | |
ID/Acronym/Agency:
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5UL1RR024143-02/RR/NCRR NIH HHS; UL1 RR024143-02/RR/NCRR NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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