Evidence map›Paper›PMID 21388663›Full record

ArticleThe Journal of allergy and clinical immunology2011

Nonlesional atopic dermatitis skin is characterized by broad terminal differentiation defects and variable immune abnormalities.

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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Article in The Journal of allergy and clinical immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

201 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  10. Functional Genetic Variation in Ubiquitin D Promoter Influences Susceptibility to Atopic Dermatitis.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026
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141 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Mayte Suárez-FariñasLaboratory for Investigative Dermatology, Rockefeller University, New York, NY 10065, USA.
Suzanne J Tintle
Avner Shemer
Andrea Chiricozzi
Kristine Nograles
Irma Cardinale
Shenghui Duan
Anne M Bowcock
James G Krueger
Emma Guttman-Yassky

Funding

TRANSFORMING TRANSLATIONAL SCIENCE AND EDUCATION TO BENEFIT HUMAN HEALTHUL1RR024143 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2006 to 2011
$49.1M
NCRR NIH HHS 5UL1RR024143-02NCRR NIH HHS UL1 RR024143
6 · The paper itself

Abstract

backgroundAtopic 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.

objectiveWe 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.

methodsWe performed genomic and histologic profiling of both ANL and AL skin lesions (n = 12 each) compared with normal human skin (n = 10).

resultsWe 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."

conclusionOur 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.

Indexed as

Gene Expression ProfilingAdolescentAdultAgedAged, 80 and overCell DifferentiationDermatitis, AtopicFemaleHumansImmunohistochemistryKeratinocytesMaleMiddle AgedOligonucleotide Array Sequence AnalysisPhenotypeReverse Transcriptase Polymerase Chain Reaction

Identifiers

PMID21388663
PMCPMC3128983

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.