Evidence map›Paper›PMID 31738991›Full record

ArticleThe Journal of allergy and clinical immunology2020

Autophagy is critical for group 2 innate lymphoid cell metabolic homeostasis and effector function.

Lauriane Galle-Treger, Benjamin P Hurrell, Gavin Lewis, Emily Howard, Pedram Shafiei Jahani, Homayon Banie, Babak Razani, Pejman Soroosh, Omid Akbari

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
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  7. The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025
    Review
  9. Dysregulation of PKM2 promotes inflammatory response in allergic rhinitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  10. Review
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  13. Article
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  15. Multifaceted roles of mitochondria in asthma.Cell biology and toxicology · 2024
    Review
  16. Article
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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

9 authors at 3 institutions in 2 countries.

Lauriane Galle-TregerDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Calif.
Benjamin P HurrellDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Calif.
Gavin LewisJanssen Research and Development, San Diego, Calif.
Emily HowardDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Calif.
Pedram Shafiei JahaniDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Calif.
Homayon BanieJanssen Research and Development, San Diego, Calif.
Babak RazaniDepartments of Medicine and Pathology & Immunology, Washington University School of Medicine and John Cochran VA Medical Center, St Louis, Mo.
Pejman SorooshJanssen Research and Development, San Diego, Calif.
Omid AkbariDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, Calif. Electronic address: akbari@usc.edu.
University of Southern California · USJanssen (Switzerland) · CHJohn Cochran VA Medical Center · US

Funding

THE ROLE OF MACROPHAGE LYSOSOMAL BIOGENESIS IN ATHEROSCLEROSISR01HL125838 · NHLBI · WASHINGTON UNIVERSITY · PI RAZANI, BABAK · 2015 to 2025
$4.6M
INTEGRATIVE GENETIC APPROACHES TO GENE-AIR POLLUTION INTERACTIONS IN ASTHMAR01ES021801 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID, ALLAYEE, HOOMAN · 2012 to 2016
$3.9M
Genetic and Environmental Determinants of Asthma EndophenotypesR01ES025786 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID, ALLAYEE, HOOMAN · 2015 to 2019
$2.8M
Induction of cells and pathways that promote respiratory tolerance in allergic asthmaR01HL144790 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID · 2019 to 2022
$2.6M
The function of CRAC channels in airway inflammationR21AI109059 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AKBARI, OMID, GWACK, YOUSANG · 2016 to 2017
$445k
Harnessing the Autophagy-Lysosomal Biogenesis Response in Macrophages to Treat AtherosclerosisI01BX003415 · VA · VETERANS HEALTH ADMINISTRATION · PI RAZANI, BABAK · 2018 to 2025
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BLRD VA I01 BX003415NHLBI NIH HHS R01 HL125838NHLBI NIH HHS R01 HL144790NIAID NIH HHS R21 AI109059NIEHS NIH HHS R01 ES021801NIEHS NIH HHS R01 ES025786
6 · The paper itself

Abstract

backgroundAllergic asthma is a chronic inflammatory disorder characterized by airway hyperreactivity (AHR) and driven by T

objectiveWe characterized the effects of autophagy deficiency on ILC2 effector functions and metabolic balance.

methodsILC2s from autophagy-deficient mice were isolated to evaluate proliferation, apoptosis, cytokine secretion, gene expression and cell metabolism. Also, autophagy-deficient ILC2s were adoptively transferred into Rag

resultsWe demonstrate that autophagy is extensively used by activated ILC2s to maintain their homeostasis and effector functions. Deletion of the critical autophagy gene autophagy-related 5 (Atg5) resulted in decreased cytokine secretion and increased apoptosis. Moreover, lack of autophagy among ILC2s impaired their ability to use fatty acid oxidation and strikingly promoted glycolysis, as evidenced by our transcriptomic and metabolite analyses. This shift of fuel dependency led to impaired homeostasis and T

conclusionThese findings provide new insights into the metabolic profile of ILC2s and suggest that modulation of fuel dependency by autophagy is a potentially new therapeutic approach to target ILC2-dependent inflammation.

Indexed as

AnimalsAutophagyHomeostasisImmunity, InnateLymphocytesMiceRespiratory Hypersensitivityairway hyperreactivityautophagyGroup 2 innate lymphoid cellsimmune metabolism

Identifiers

PMID31738991
PMCPMC7010567
OpenAlexW2987088395

What OpenQuestion holds

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LicenceTDM
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.