Evidence map›Paper›PMID 39352743›Full record

ArticleJCI insight2024

The DNA sensor AIM2 mediates psoriasiform inflammation by inducing type 3 immunity.

Timna Varela Martins, Bruno Marcel Silva de Melo, Juliana Escher Toller-Kawahisa, Gabriel Victor Lucena da Silva, Conceição Elidianne Aníbal Silva, Isadora Marques Paiva, Gabriel Azevedo Públio, Marcos Henrique Rosa, Cacilda da Silva Souza, Dario Simões Zamboni and 5 more

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. [Gut-brain-joint axis in rheumatoid arthritis: from microeco-logical disturbance to multi-target synergy].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. 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

15 authors.

Timna Varela MartinsDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Bruno Marcel Silva de MeloDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Juliana Escher Toller-KawahisaCenter for Research in Inflammatory Diseases, Ribeirão Preto Medical School, University of Sao Paulo, Ribeirão Preto, Sao Paulo, Brazil.
Gabriel Victor Lucena da SilvaDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Conceição Elidianne Aníbal SilvaDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Isadora Marques PaivaDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Gabriel Azevedo PúblioDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Marcos Henrique RosaDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Cacilda da Silva SouzaDermatology division, Ribeirão Preto Clinical Hospital, Sao Paulo, Brazil.
Dario Simões ZamboniDepartment of Cell Biology, Ribeirão Preto Medical School, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.
Fernando Q CunhaDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Thiago Mattar CunhaDepartment of Pharmacology, Ribeirão Preto Medical School, and.
Bernhard RyffelINEM, CNRS, UMR7355 and University, Orleans, France.
Nicolas RiteauImmune Health Laboratory, Regulation of host responses and immune health, IRL2029, French National Centre for Scientific Research (CNRS) and Ribeirão Preto Medical School (FMRP) of the Sao Paulo University (USP), Sao Paulo, Brazil.
José C Alves-FilhoDepartment of Pharmacology, Ribeirão Preto Medical School, and.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic and recurrent inflammatory skin disease characterized by abnormal proliferation and differentiation of keratinocytes and activation of immune cells. However, the molecular driver that triggers this immune response in psoriatic skin remains unclear. The inflammation-related gene absent in melanoma 2 (AIM2) was identified as a susceptibility gene/locus associated with psoriasis. In this study, we investigated the role of AIM2 in the pathophysiology of psoriasis. We found elevated levels of mitochondrial DNA in patients with psoriasis, along with high expression of AIM2 in both the human psoriatic epidermis and a mouse model of psoriasis induced by topical imiquimod (IMQ) application. Genetic ablation of AIM2 reduced the development of IMQ-induced psoriasis by decreasing the production of type 3 cytokines (such as IL-17A and IL-23) and infiltration of immune cells into the inflammatory site. Furthermore, we demonstrate that IL-17A induced AIM2 expression in keratinocytes. Finally, the genetic absence of inflammasome components downstream AIM2, ASC, and caspase-1 alleviated IMQ-induced skin inflammation. Collectively, our data show that AIM2 is involved in developing psoriasis through its canonical activation.

Indexed as

Disease Models, AnimalDNA-Binding ProteinsImiquimodInflammasomesInterleukin-17KeratinocytesPsoriasisAnimalsDNA, MitochondrialFemaleHumansInflammationInterleukin-23MaleMiceMice, KnockoutAIM2 protein, humanAim2 protein, mouseDNA-Binding ProteinsDNA, MitochondrialImiquimodInflammasomesInterleukin-17Interleukin-23InflammationSkin

Identifiers

PMID39352743
PMCPMC11601563

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Registered trials

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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.