Evidence map›Paper›PMID 30984196›Full record

ArticleFrontiers in immunology2019

Non-cytotoxic Cardiac Innate Lymphoid Cells Are a Resident and Quiescent Type 2-Commited Population.

William Bracamonte-Baran, Guobao Chen, Xuezhou Hou, Monica V Talor, Hee Sun Choi, Giovanni Davogustto, Heinrich Taegtmeyer, Jungeun Sung, David Joel Hackam, David Nauen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.5field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
  2. Review
  3. Article
  4. Frontiers in immunology · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  13. Article
  14. Immune cells in cardiac repair and regeneration.Development (Cambridge, England) · 2022
    Review
  15. Review
  16. Review
  17. Review
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  20. 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

11 authors at 3 institutions in 1 country.

William Bracamonte-BaranDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Guobao ChenDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Xuezhou HouW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States.
Monica V TalorDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Hee Sun ChoiDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Giovanni DavogusttoDivision of Cardiology, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, TX, United States.
Heinrich TaegtmeyerDivision of Cardiology, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, TX, United States.
Jungeun SungSchool of Medicine, Institute of Genetic Medicine, Johns Hopkins University, Baltimore, MD, United States.
David Joel HackamDivision of General Pediatric Surgery, Johns Hopkins University and Bloomberg Children's Center, Johns Hopkins Hospital, Baltimore, MD, United States.
David NauenDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Daniela ČihákováDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD, United States.
Johns Hopkins University · USJohns Hopkins Medicine · USJohns Hopkins Hospital · US

Funding

SWITCHING OF METABOLIC GENES IN UNLOADED HEARTR01HL061483 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 1999 to 2021
$6.2M
Myeloid Cells are Critical in Inflammatory Heart DiseaseR01HL118183 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2014 to 2023
$4.4M
TLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9M
Modulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4M
Role of Sca-1+Cardiac Fibroblasts in Inflammatory Heart Disease`R01HL136586 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2018 to 2021
$1.6M
Eosinophilic MyocarditisR01HL113008 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2012 to 2015
$1.6M
Maternal-Fetal AHR Signaling in the Pathogenesis and Treatment of Necrotizing EnterocolitisR01DK117186 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI HACKAM, DAVID J · 2018 to 2021
$1.5M
NHLBI NIH HHS R01 HL061483NHLBI NIH HHS R01 HL113008NHLBI NIH HHS R01 HL118183NHLBI NIH HHS R01 HL136586NIDDK NIH HHS R01 DK083752NIDDK NIH HHS R01 DK117186
6 · The paper itself

Abstract

Innate lymphoid cells (ILC) are a subset of leukocytes with lymphoid properties that lack antigen specific receptors. They can be stimulated by and exert their effect via specific cytokine axes, whereas Natural Killers (NK) cells are the only known cytotoxic member of this family. ILCs are considered key in linking the innate and adaptive response in physiologic and pathologic environments. In this study, we investigated the properties of non-cytotoxic cardiac ILCs in physiologic, inflammatory, and ischemic conditions. We found that in healthy humans and mice, non-cytotoxic cardiac ILCs are predominantly a type 2-committed population with progenitor-like features, such as an absence of type-specific immunophenotype, intermediate GATA3 expression, and capacity to transiently express Pro-myelocytic Leukemia Zinc Finger protein (PLZF) upon activation. During myocarditis and ischemia, in both human and mice, cardiac ILCs differentiated into conventional ILC2s. We found that cardiac ILCs lack IL-25 receptor and cannot become inflammatory ILC2s. We found a strong correlation between IL-33 production in the heart and the ability of cardiac ILCs to become conventional ILC2s. The main producer of IL-33 was a subset of CD29+Sca-1+ cardiac fibroblasts. ILC2 expansion and fibroblast-derived IL-33 production were significantly increased in the heart in mouse models of infarction and myocarditis. Despite its progenitor-like status in healthy hearts, cardiac ILCs were unable to become ILC1 or ILC3

Indexed as

Immunity, InnateAnimalsFemaleFibroblastsGATA3 Transcription FactorGene Expression RegulationHumansInterleukin-33Killer Cells, NaturalMaleMiceMice, KnockoutMyocardial IschemiaMyocarditisMyocardiumPromyelocytic Leukemia Zinc Finger ProteinGATA3 protein, humanGata3 protein, mouseGATA3 Transcription FactorIL33 protein, humanIl33 protein, mouseInterleukin-33Promyelocytic Leukemia Zinc Finger ProteinZBTB16 protein, humanZbtb16 protein, mousefibroblastsheartIL-33innate lymphoid cellsmyocardial infarctionmyocarditis

Identifiers

PMID30984196
PMCPMC6450181
OpenAlexW2925845275

What OpenQuestion holds

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LicenceCC BY
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.