Evidence map›Paper›PMID 32075728›Full record

ArticleImmunity2020

Insulin-like Growth Factor 1 Supports a Pulmonary Niche that Promotes Type 3 Innate Lymphoid Cell Development in Newborn Lungs.

Katherine Oherle, Elizabeth Acker, Madeline Bonfield, Timothy Wang, Jerilyn Gray, Ian Lang, James Bridges, Ian Lewkowich, Yan Xu, Shawn Ahlfeld and 3 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  7. Article
  8. Insulin signaling in development.Development (Cambridge, England) · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Katherine OherleDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA.
Elizabeth AckerDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA.
Madeline BonfieldDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Immunology Graduate Program, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Timothy WangDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Jerilyn GrayDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA.
Ian LangDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA.
James BridgesDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Ian LewkowichDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Yan XuDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Shawn AhlfeldDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
William ZachariasDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Theresa AlenghatDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Hitesh DeshmukhDivision of Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45219, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA. Electronic address: hitesh.deshmukh@cchmc.org.
Cincinnati Children's Hospital Medical Center · US

Funding

Host integration of commensal and pathogenic bacterial-derived signalsR01DK116868 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Theresa Alenghat · 2018 to 2026
$4.1M
"Lung MAP" Atlas Research CenterU01HL122642 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI POTTER, S. STEVEN, WHITSETT, JEFFREY A · 2014 to 2018
$3.9M
Mechanisms of IL-17A-mediated enhancement of asthma severityR01HL122300 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI LEWKOWICH, IAN PAUL · 2014 to 2018
$2.2M
Development of neonatal innate lung defenses is dependent on gastrointestinal commensal bacteriaR01HL142708 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI DESHMUKH, HITESH · 2018 to 2022
$2.1M
Role of GPR116 in Alveolar HomeostasisR01HL131634 · NHLBI · NATIONAL JEWISH HEALTH · PI BRIDGES, JAMES PATRICK · 2016 to 2020
$2.0M
Tissue niches for ILC3 development in newborn's lungR01HL155611 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI DESHMUKH, HITESH · 2021 to 2024
$1.9M
Epigenomic control of antimicrobial immunity in the intestineR01DK114123 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ALENGHAT, THERESA · 2018 to 2022
$1.8M
Mechanistic evaluation of a novel Wnt-responsive adult alveolar epithelial progenitor population during regeneration after diffuse alveolar damageK08HL140178 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ZACHARIAS, WILLIAM JOHN · 2018 to 2022
$815k
Epigenetic regulation of intestinal homeostasisK08DK093784 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI ALENGHAT, THERESA · 2012 to 2016
$764k
Role of commensal bacteria in regulating neutrophil-mediated host defense in neonatesK08HD084686 · NICHD · CINCINNATI CHILDRENS HOSP MED CTR · PI DESHMUKH, HITESH · 2015 to 2018
$586k
A pilot study to target out-of-dialysis-unit versus dialysis-unit blood pressureR21DK114213 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BANSAL, NISHA, HSU, CHI-YUAN · 2017 to 2018
$456k
NHLBI NIH HHS K08 HL140178NHLBI NIH HHS R01 HL122300NHLBI NIH HHS R01 HL131634NHLBI NIH HHS R01 HL142708NHLBI NIH HHS R01 HL155611NHLBI NIH HHS U01 HL122642NICHD NIH HHS K08 HD084686NIDDK NIH HHS K08 DK093784NIDDK NIH HHS R01 DK114123NIDDK NIH HHS R01 DK116868NIDDK NIH HHS R21 DK114213
6 · The paper itself

Abstract

Type 3 innate lymphoid cells (ILC3s) are critical for lung defense against bacterial pneumonia in the neonatal period, but the signals that guide pulmonary ILC3 development remain unclear. Here, we demonstrated that pulmonary ILC3s descended from ILC precursors that populated a niche defined by fibroblasts in the developing lung. Alveolar fibroblasts produced insulin-like growth factor 1 (IGF1), which instructed expansion and maturation of pulmonary ILC precursors. Conditional ablation of IGF1 in alveolar fibroblasts or deletion of the IGF-1 receptor from ILC precursors interrupted ILC3 biogenesis and rendered newborn mice susceptible to pneumonia. Premature infants with bronchopulmonary dysplasia, characterized by interrupted postnatal alveolar development and increased morbidity to respiratory infections, had reduced IGF1 concentrations and pulmonary ILC3 numbers. These findings indicate that the newborn period is a critical window in pulmonary immunity development, and disrupted lung development in prematurely born infants may have enduring effects on host resistance to respiratory infections.

Indexed as

Immunity, InnateAlveolar Epithelial CellsAnimalsAnimals, NewbornBronchopulmonary DysplasiaCell DifferentiationCell ProliferationDisease SusceptibilityHumansInfant, NewbornInfant, PrematureInsulin-Like Growth Factor IInterleukin-22InterleukinsLungLymphocytesIgf1r protein, mouseinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IInterleukin-22InterleukinsPromyelocytic Leukemia Zinc Finger ProteinReceptor, IGF Type 1Receptor, Platelet-Derived Growth Factor alphaZbtb16 protein, mouseILC3 biogenesislung developmentlung resistance

Identifiers

PMID32075728
PMCPMC7382307
OpenAlexW3008528752

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.