Evidence map›Paper›PMID 35596901›Full record

ReviewDermatology and therapy2022

Current and Emerging Strategies to Inhibit Type 2 Inflammation in Atopic Dermatitis.

El-Bdaoui Haddad, Sonya L Cyr, Kazuhiko Arima, Robert A McDonald, Noah A Levit, Frank O Nestle

Open access · goldAbstract readReview
In one paragraph

Review in Dermatology and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% of its field
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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Defining the Potential for Disease Modification in Atopic Dermatitis.American journal of clinical dermatology · 2026
    Review
  9. Review
  10. Review
  11. Incidence of autoimmune diseases in children with atopy treated with dupilumab.The Journal of allergy and clinical immunology · 2026
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Sexual Dimorphism in Allergic and Mast Cell-Associated Diseases.Clinical reviews in allergy & immunology · 2026
    Review
  18. Article
  19. Article
  20. Review

1 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

6 authors at 5 institutions in 4 countries.

El-Bdaoui Haddad *Sanofi, 450 Water Street, Cambridge, MA, USA. El-Bdaoui.Haddad@sanofi.com.
Sonya L Cyr *Regeneron Pharmaceuticals, Inc., Tarrytown, NY, USA.
Kazuhiko ArimaSanofi, Tokyo, Japan.ORCID http://orcid.org/0000-0002-0607-8787
Robert A McDonaldSanofi, Reading, Berkshire, UK.
Noah A LevitRegeneron Pharmaceuticals, Inc., Tarrytown, NY, USA.ORCID http://orcid.org/0000-0002-0797-5121
Frank O NestleSanofi, 450 Water Street, Cambridge, MA, USA.
Regeneron (United States) · USSanofi (France) · FRSanofi (Japan) · JPSanofi (United Kingdom) · GBSanofi (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 immunity evolved to combat helminth infections by orchestrating a combined protective response of innate and adaptive immune cells and promotion of parasitic worm destruction or expulsion, wound repair, and barrier function. Aberrant type 2 immune responses are associated with allergic conditions characterized by chronic tissue inflammation, including atopic dermatitis (AD) and asthma. Signature cytokines of type 2 immunity include interleukin (IL)-4, IL-5, IL-9, IL-13, and IL-31, mainly secreted from immune cells, as well as IL-25, IL-33, and thymic stromal lymphopoietin, mainly secreted from tissue cells, particularly epithelial cells. IL-4 and IL-13 are key players mediating the prototypical type 2 response; IL-4 initiates and promotes differentiation and proliferation of naïve T-helper (Th) cells toward a Th2 cell phenotype, whereas IL-13 has a pleiotropic effect on type 2 inflammation, including, together with IL-4, decreased barrier function. Both cytokines are implicated in B-cell isotype class switching to generate immunoglobulin E, tissue fibrosis, and pruritus. IL-5, a key regulator of eosinophils, is responsible for eosinophil growth, differentiation, survival, and mobilization. In AD, IL-4, IL-13, and IL-31 are associated with sensory nerve sensitization and itch, leading to scratching that further exacerbates inflammation and barrier dysfunction. Various strategies have emerged to suppress type 2 inflammation, including biologics targeting cytokines or their receptors, and Janus kinase inhibitors that block intracellular cytokine signaling pathways. Here we review type 2 inflammation, its role in inflammatory diseases, and current and future therapies targeting type 2 pathways, with a focus on AD. INFOGRAPHIC.

Indexed as

Atopic dermatitisBiologicCytokineJanus kinaseType 2 inflammation

Identifiers

PMID35596901
PMCPMC9276864
OpenAlexW4281262324

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.