Evidence map›Paper›PMID 24030647›Full record

ArticleThe Journal of investigative dermatology2013

Mechanisms of contact sensitization offer insights into the role of barrier defects vs. intrinsic immune abnormalities as drivers of atopic dermatitis.

Nikhil Dhingra, Nicholas Gulati, Emma Guttman-Yassky

Abstract readComment
In one paragraph

Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

  1. Article
  2. Beyond Avoidance: Advanced Therapies for Contact Dermatitis.The journal of allergy and clinical immunology. In practice · 2024
    Review
  3. Experimental and therapeutic medicine · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Anti-inflammatory effect of aged black garlic on 12-Nutrition research and practice · 2019
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Anti-inflammatory effect of galectin-1 in a murine model of atopic dermatitis.Journal of molecular medicine (Berlin, Germany) · 2017
    Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Nikhil DhingraLaboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA; Columbia University College of Physicians and Surgeons, New York, New York, USA.
Nicholas GulatiLaboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA.
Emma Guttman-YasskyLaboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Electronic address: Emma.Guttman@mountsinai.org.

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
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 RR024143NIGMS NIH HHS GM07739NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by wet, oozing, erythematous, pruritic lesions in the acute stage and xerotic, lichenified plaques in the chronic stage. It frequently coexists with asthma and allergic rhinitis, sharing some mechanistic features with these diseases as part of the "atopic march." Controversy exists as to whether immune abnormalities, epidermal barrier defects, or both are the primary factors responsible for disease pathogenesis. In AD patients, there is often a coexisting irritant contact dermatitis (ICD) or allergic contact dermatitis (ACD) that is sometimes clinically difficult to distinguish from AD. ACD shares molecular mechanisms with AD, including increased cellular infiltrates and cytokine activation (Gittler et al., 2013). In this issue, Newell et al. (2013) used an experimental contact sensitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype of AD patients.

Indexed as

Dermatitis, Allergic ContactDermatitis, AtopicFemaleHumansMaleSkinTh2 Cells

Identifiers

PMID24030647
PMCPMC3773606

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.