Evidence map›Paper›PMID 34276687›Full record

ReviewFrontiers in immunology2021

Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis.

Jianghui Meng, Yanqing Li, Michael J M Fischer, Martin Steinhoff, Weiwei Chen, Jiafu Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
15.2field-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

65 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Monoclonal Antibodies in Pediatric Atopic Dermatitis; Efficacy and Safety.Current therapeutic research, clinical and experimental · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. The stem ofFrontiers in immunology · 2026
    Article
  11. Skin innervation and itsFrontiers in cellular neuroscience · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

5 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 3 institutions in 5 countries.

Jianghui MengSchool of Life Sciences, Henan University, Kaifeng, China.
Yanqing LiSchool of Life Sciences, Henan University, Kaifeng, China.
Michael J M FischerCenter for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Martin SteinhoffDepartment of Dermatology and Venereology, Hamad Medical Corporation, Doha, Qatar.
Weiwei ChenSchool of Life Sciences, Henan University, Kaifeng, China.
Jiafu WangSchool of Life Sciences, Henan University, Kaifeng, China.
Henan University · CNCornell University · USMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a multifaceted, chronic relapsing inflammatory skin disease that affects people of all ages. It is characterized by chronic eczema, constant pruritus, and severe discomfort. AD often progresses from mild annoyance to intractable pruritic inflammatory lesions associated with exacerbated skin sensitivity. The T helper-2 (Th2) response is mainly linked to the acute and subacute phase, whereas Th1 response has been associated in addition with the chronic phase. IL-17, IL-22, TSLP, and IL-31 also play a role in AD. Transient receptor potential (TRP) cation channels play a significant role in neuroinflammation, itch and pain, indicating neuroimmune circuits in AD. However, the Th2-driven cutaneous sensitization of TRP channels is underappreciated. Emerging findings suggest that critical Th2-related cytokines cause potentiation of TRP channels, thereby exaggerating inflammation and itch sensation. Evidence involves the following: (i) IL-13 enhances TRPV1 and TRPA1 transcription levels; (ii) IL-31 sensitizes TRPV1

Indexed as

AnimalsAnti-Inflammatory AgentsCytokinesDermatitis, AtopicDisease ProgressionHumansInflammation MediatorsMembrane Transport ModulatorsMolecular Targeted TherapyPruritusSignal TransductionSkinTh2 CellsTranscriptional ActivationTransient Receptor Potential ChannelsAnti-Inflammatory AgentsCytokinesInflammation MediatorsMembrane Transport ModulatorsTransient Receptor Potential Channelsinterleukin-13interleukin-31itchprotease activated receptor 2pruritusT helper-2thymic stromal lymphopoietintransient receptor potential channel

Identifiers

PMID34276687
PMCPMC8278285
OpenAlexW3176794103

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.