Evidence map›Paper›PMID 38752989›Full record

ArticleProtein & cell2025

IL-24 promotes atopic dermatitis-like inflammation through driving MRSA-induced allergic responses.

Xinmin Qian, Meiyi Tong, Tianqing Zhang, Qingqing Li, Meng Hua, Nan Zhou, Wenwen Zeng

Abstract read
In one paragraph

Article in Protein & cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Interleukin-24 in type 2 immune diseases.Frontiers in immunology · 2026
    Review
  4. Article
  5. Skin-lung axis in the atopic march: The immune link from skin to lungs.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  6. Review
  7. Article
  8. Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  9. Article
  10. 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

7 authors.

Xinmin QianInstitute for Immunology and School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing 100084, China.ORCID 0000-0003-1317-9292
Meiyi TongEight-year Medical Doctor Program, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100084, China.ORCID 0009-0005-2785-9418
Tianqing ZhangSchool of Life Sciences, Tsinghua University, Beijing 100084, China.ORCID 0000-0002-8783-4416
Qingqing LiInstitute for Immunology and School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing 100084, China.ORCID 0000-0001-5496-6044
Meng HuaInstitute for Immunology and School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing 100084, China.
Nan ZhouInstitute for Immunology and School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing 100084, China.
Wenwen ZengInstitute for Immunology and School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing 100084, China.ORCID 0000-0001-8544-3318

Funding

National Key R&D Program of China 2023YFC2306300National Natural Science Foundation of China 32225019, 92357304, and 32394003
6 · The paper itself

Abstract

Atopic dermatitis (AD) is a prevalent inflammatory skin disorder in which patients experience recurrent eczematous lesions and intense itching. The colonization of Staphylococcus aureus (S. aureus) is correlated with the severity of the disease, but its role in AD development remains elusive. Using single-cell RNA sequencing, we uncovered that keratinocytes activate a distinct immune response characterized by induction of Il24 when exposed to methicillin-resistant S. aureus (MRSA). Further experiments using animal models showed that the administration of recombinant IL-24 protein worsened AD-like pathology. Genetic ablation of Il24 or the receptor Il20rb in keratinocytes alleviated allergic inflammation and atopic march. Mechanistically, IL-24 acted through its heterodimeric receptors on keratinocytes and augmented the production of IL-33, which in turn aggravated type 2 immunity and AD-like skin conditions. Overall, these findings establish IL-24 as a critical factor for onset and progression of AD and a compelling therapeutic target.

Indexed as

Dermatitis, AtopicHypersensitivityInflammationInterleukinsMethicillin-Resistant Staphylococcus aureusStaphylococcal InfectionsAnimalsDisease Models, AnimalHumansInterleukin-24Interleukin-33KeratinocytesMiceMice, Inbred C57BLInterleukin-24Interleukin-33Interleukinsallergic inflammationatopic dermatitisIL-24keratinocytesMRSA

Identifiers

PMID38752989
PMCPMC11892005

What OpenQuestion holds

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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.