Evidence map›Paper›PMID 33106586›Full record

ArticleMucosal immunology2021

Metabolic regulation by PPARγ is required for IL-33-mediated activation of ILC2s in lung and adipose tissue.

Tinhinane Fali, Tegest Aychek, Maroua Ferhat, Jean-Yves Jouzeau, Meinrad Busslinger, David Moulin, Gérard Eberl

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Review
  7. Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. ILC2s - development, divergence, dispersal.Current opinion in immunology · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Tinhinane Fali *Institut Pasteur, Microenvironment & Immunity Unit, 75724, Paris, France.
Tegest Aychek *Institut Pasteur, Microenvironment & Immunity Unit, 75724, Paris, France.
Maroua FerhatIMoPA, UMR7365 CNRS-Université de Lorraine, Vandœuvre-lès-Nancy, France.
Jean-Yves JouzeauIMoPA, UMR7365 CNRS-Université de Lorraine, Vandœuvre-lès-Nancy, France.
Meinrad BusslingerResearch Institute of Molecular Pathology, Vienna Biocenter, Campus-Vienna-Biocenter 1, Vienna, Austria.
David MoulinIMoPA, UMR7365 CNRS-Université de Lorraine, Vandœuvre-lès-Nancy, France. david.moulin@univ-lorraine.fr.ORCID http://orcid.org/0000-0001-6619-5769
Gérard EberlInstitut Pasteur, Microenvironment & Immunity Unit, 75724, Paris, France. gerard.eberl@pasteur.fr.ORCID http://orcid.org/0000-0002-1119-5638
Inserm · FRIngénierie Moléculaire et Physiopathologie Articulaire · FRCentre National de la Recherche Scientifique · FRResearch Institute of Molecular Pathology · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 innate lymphoid cells (ILC2s) play a critical role early in the response to infection by helminths and in the development of allergic reactions. ILC2s are also involved in the physiologic regulation of adipose tissue and its metabolic response to cold shock. We find that the metabolic sensor peroxisome proliferator-activated receptor gamma (PPARγ) is highly expressed in ILC2s of the lung and adipose tissue and increases responsiveness to IL-33. In turn, activation of ILC2 by IL-33 leads to increased expression of PPARγ, a prerequisite for proliferation and expression of the effector cytokines IL-5 and IL-13. In contrast, pharmacological inhibition of PPARγ leads to decreased expression of CD36 and fatty acid uptake, a necessary source of energy for ILC2s and of potential ligands for PPARγ. As a consequence, treatment of mice with a PPARγ antagonist reduces the severity of an ILC2-dependent acute airway inflammation. Together, our results demonstrate the critical role of the metabolic sensor PPARγ for the functions of ILC2s.

Indexed as

Adipose TissueAnimalsCD36 AntigensCells, CulturedCytokinesDown-RegulationHumansInterleukin-33LungLymphocytesMiceMice, Inbred C57BLMice, KnockoutPneumoniaPPAR gammaRespiratory HypersensitivityCD36 AntigensCytokinesInterleukin-33PPAR gamma

Identifiers

PMID33106586
OpenAlexW3094040964

What OpenQuestion holds

Textmetadata
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.