Evidence map›Paper›PMID 33852849›Full record

ArticleCell reports2021

A stromal progenitor and ILC2 niche promotes muscle eosinophilia and fibrosis-associated gene expression.

Jenna M Kastenschmidt, Gerald Coulis, Philip K Farahat, Phillip Pham, Rodolfo Rios, Therese T Cristal, Ali H Mannaa, Rachel E Ayer, Rayan Yahia, Archis A Deshpande and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Fibrotic chronic eosinophilic pneumonia: from inflammation to fibrosis and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  4. Article
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  6. Review
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  9. Article
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  11. PdgfrαGenes & diseases · 2025
    Review
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  14. Article
  15. 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

17 authors at 3 institutions in 1 country.

Jenna M KastenschmidtDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA; Institute for Immunology, University of California Irvine, Irvine, CA, USA.
Gerald CoulisDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA; Institute for Immunology, University of California Irvine, Irvine, CA, USA.
Philip K FarahatDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA; Institute for Immunology, University of California Irvine, Irvine, CA, USA.
Phillip PhamDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Rodolfo RiosDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Therese T CristalDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Ali H MannaaDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Rachel E AyerDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Rayan YahiaDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Archis A DeshpandeDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Brandon S HughesDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA.
Adam K SavageHoward Hughes Medical Institute, University of California San Francisco, San Francisco, CA, USA; Departments of Medicine and Microbiology & Immunology, University of California San Francisco, San Francisco, CA, USA.
Carlee R GiesigeBiomedical Sciences Graduate Program, The Ohio State University, Columbus, OH, USA; Center for Gene Therapy, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
Scott Q HarperBiomedical Sciences Graduate Program, The Ohio State University, Columbus, OH, USA; Center for Gene Therapy, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA; Department of Pediatrics, The Ohio State University, Columbus, OH, USA.
Richard M LocksleyHoward Hughes Medical Institute, University of California San Francisco, San Francisco, CA, USA.
Tahseen MozaffarInstitute for Immunology, University of California Irvine, Irvine, CA, USA; Department of Neurology, University of California Irvine, Irvine, CA, USA; Department of Orthopaedic Surgery, University of California Irvine, Irvine, CA, USA; Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA, USA.
S Armando VillaltaDepartment of Physiology and Biophysics, University of California Irvine, Irvine, CA, USA; Institute for Immunology, University of California Irvine, Irvine, CA, USA; Department of Neurology, University of California Irvine, Irvine, CA, USA. Electronic address: armando.villalta@uci.edu.
University of California, Irvine · USNationwide Children's Hospital · USUniversity of California, San Francisco · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
Role of miRNAs in Th2-Driven inflammation in AsthmaP01HL107202 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FAHY, JOHN V · 2012 to 2023
$23.3M
Training Core [Parent Title: NOVEL THERAPEUTICS FOR FSHD]P50HD060848 · NICHD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI EMERSON, CHARLES P. · 2018 to 2023
$8.6M
Project 3: Use of an IRES-driven N-truncated dystrophin isoform as a clinical therapy for 5 mutations in the dystrophinopathiesP50AR070604 · NIAMS · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI MCBRIDE, KIM LEWIS · 2016 to 2020
$7.3M
Institutional Career Development CoreKL2TR001416 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI CAIOZZO, VINCENT JAMES, DEMETRIOU, MICHAEL · 2015 to 2023
$5.6M
Novel macrophage and regulatory T cell interactions that promote the pathogenesis of Duchenne muscular dystrophyR01NS120060 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI VILLALTA, SERGIO ARMANDO · 2020 to 2024
$2.5M
Immunology Research Training ProgramT32AI060573 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI PEARLMAN, ERIC · 2005 to 2020
$1.9M
DUX4 and the P53 pathway in FSHD pathogenesisR01AR062123 · NIAMS · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI HARPER, SCOTT Q · 2012 to 2016
$1.6M
The Ohio State University Center for Clinical and Translational ScienceTL1TR001069 · NCATS · OHIO STATE UNIVERSITY · PI JACKSON, REBECCA D · 2013 to 2017
$763k
Group 2 innate lymphoid cells in tissue regenerationR21AI134657 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI VILLALTA, SERGIO ARMANDO · 2017 to 2018
$406k
Howard Hughes Medical InstituteNCATS NIH HHS KL2 TR001416NCATS NIH HHS TL1 TR001069NCATS NIH HHS UL1 TR001414NHLBI NIH HHS P01 HL107202NIAID NIH HHS R21 AI134657NIAID NIH HHS T32 AI060573NIAMS NIH HHS P50 AR070604NIAMS NIH HHS R01 AR062123NICHD NIH HHS P50 HD060848NINDS NIH HHS R01 NS120060
6 · The paper itself

Abstract

Despite the well-accepted view that chronic inflammation contributes to the pathogenesis of Duchenne muscular dystrophy (DMD), the function and regulation of eosinophils remain an unclear facet of type II innate immunity in dystrophic muscle. We report the observation that group 2 innate lymphoid cells (ILC2s) are present in skeletal muscle and are the principal regulators of muscle eosinophils during muscular dystrophy. Eosinophils were elevated in DMD patients and dystrophic mice along with interleukin (IL)-5, a major eosinophil survival factor that was predominantly expressed by muscle ILC2s. We also find that IL-33 was upregulated in dystrophic muscle and was predominantly produced by fibrogenic/adipogenic progenitors (FAPs). Exogenous IL-33 and IL-2 complex (IL-2c) expanded muscle ILC2s and eosinophils, decreased the cross-sectional area (CSA) of regenerating myofibers, and increased the expression of genes associated with muscle fibrosis. The deletion of ILC2s in dystrophic mice mitigated muscle eosinophilia and impaired the induction of IL-5 and fibrosis-associated genes. Our findings highlight a FAP/ILC2/eosinophil axis that promotes type II innate immunity, which influences the balance between regenerative and fibrotic responses during muscular dystrophy.

Indexed as

AnimalsCell ProliferationChemokines, CCEosinophilsFibroblastsFibrosisGene ExpressionGene Expression ProfilingHumansImmunity, InnateInterleukin-2Interleukin-33Interleukin-5IntestinesLungLymphocytesChemokines, CCIl33 protein, mouseInterleukin-2Interleukin-33Interleukin-5chemokineseosinophilsfibro/adipogenic progenitorsILC2interleukin-33interleukin-5muscle inflammationmuscular dystrophyST2type II innate immunity

Identifiers

PMID33852849
PMCPMC8127948
OpenAlexW3156008913

What OpenQuestion holds

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Read underepoch 390

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.