Evidence map›Paper›PMID 30619628›Full record

ReviewImmune network2018

From Bench to Clinic: the Potential of Therapeutic Targeting of the IL-22 Signaling Pathway in Atopic Dermatitis.

Mirim Jin, Juhan Yoon

Open access · hybridAbstract readReview
In one paragraph

Review in Immune network, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Memory Cells in Atopic Dermatitis: Paving the Way to Disease Modification.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Keratinocytes: innate immune cells in atopic dermatitis.Clinical and experimental immunology · 2021
    Review
  14. Immunological Aspects of Skin Aging in Atopic Dermatitis.International journal of molecular sciences · 2021
    Review
  15. Article
  16. IL-22 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Article
  17. Review
  18. Article
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

2 authors at 2 institutions in 1 country.

Mirim JinDepartment of Microbiology, College of Medicine, Gachon University, Incheon 21999, Korea.ORCID https://orcid.org/0000-0001-7268-3400
Juhan YoonDepartment of Pharmacology, C&C Research Laboratories, Suwon 16419, Korea.ORCID https://orcid.org/0000-0002-2870-796X
Gachon University · KRSuwon Research Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is the most common pruritic inflammatory skin disease characterized by thickening of epidermis and dermis as well as by the infiltration of multiple pathogenic polarized T lymphocytes, including Th2, Th17, and Th22 cells. Significant progress has been made to develop targeted therapeutics for treating AD, e.g., Food and Drug Administration-approved dupilumab, an antibody for dual targeting of IL-4 and IL-13 signaling pathways. Additionally, a growing body of published evidence and a promising result from the early stage of the clinical trial with ILV-094, an anti-IL-22 antibody, strongly support the notion that IL-22 is a potential therapeutic target for treating AD. Moreover, we also experimentally proved that IL-22 contributes to the pathophysiology of AD by employing a murine model of AD induced by epicutaneous sensitization. Here, we review recent preclinical and clinical findings that have advanced our understanding of the roles of IL-22 and Th22 cells in skin inflammation. We conclude that blockade of IL-22 signaling may be a promising therapeutic approach for the treatment of AD.

Indexed as

Atopic dermatitisIL-22Th22

Identifiers

PMID30619628
PMCPMC6312894
OpenAlexW2907446068

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.