Evidence map›Paper›PMID 33945505›Full record

ArticleJCI insight2021

Antibody-mediated depletion of CCR10+EphA3+ cells ameliorates fibrosis in IPF.

Miriam S Hohmann, David M Habiel, Milena S Espindola, Guanling Huang, Isabelle Jones, Rohan Narayanan, Ana Lucia Coelho, Justin M Oldham, Imre Noth, Shwu-Fan Ma and 12 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed, 24 citations in OpenAlex.

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  15. Cellular Senescence: Pathogenic Mechanisms in Lung Fibrosis.International journal of molecular sciences · 2021
    Review
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

22 authors at 5 institutions in 2 countries.

Miriam S HohmannWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
David M HabielWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Milena S EspindolaWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Guanling HuangWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Isabelle JonesWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Rohan NarayananWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Ana Lucia CoelhoWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Justin M OldhamDivision of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of California, Davis, Sacramento, California, USA.
Imre NothDivision of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, University of Virginia, Charlottesville, Virginia, USA.
Shwu-Fan MaDivision of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, University of Virginia, Charlottesville, Virginia, USA.
Adrianne KurkciyanWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Jonathan L McQualterWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Gianni CarraroWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Barry StrippWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Peter ChenWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Dianhua JiangWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Paul W NobleWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
William ParksWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
John WoroniczKaloBios Pharmaceuticals, Inc. (now Humanigen, Inc.), Burlingame, California, USA.
Geoffrey YarrantonKaloBios Pharmaceuticals, Inc. (now Humanigen, Inc.), Burlingame, California, USA.
Lynne A MurrayMiroBio Ltd, Oxford, United Kingdom.
Cory M HogaboamWomen's Guild Lung Institute, Division of Pulmonary and Critical Care Medicine, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Cedars-Sinai Medical Center · USHumanigen (United States) · USUniversity of Virginia · USMirada Medical (United Kingdom) · GBUniversity of California, Davis · US

Funding

Lung Immunopathology Training Stipend SupplementT32HL007517 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1985 to 2022
$6.1M
Architectural structure and regulation of TOLLIP in IPFR01HL130796 · NHLBI · UNIVERSITY OF VIRGINIA · PI NOTH, IMRE · 2016 to 2019
$3.1M
Innate DNA sensing in rapidly progressing IPFR01HL123899 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI HOGABOAM, CORY M · 2015 to 2018
$2.0M
Elucidating the Genomic Determinants of Outcomes in Idiopathic Pulmonary FibrosisK23HL138190 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OLDHAM, JUSTIN M · 2017 to 2021
$914k
Novel agents for idiopathic pulmonary fibrosisR43HL150986 · NHLBI · EPIGEN BIOSCIENCES, INC. · PI HOGABOAM, CORY M, TUCCI, FABIO COHEN · 2020 to 2020
$300k
NHLBI NIH HHS K23 HL138190NHLBI NIH HHS R01 HL123899NHLBI NIH HHS R01 HL130796NHLBI NIH HHS T32 HL007517
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant repair that diminishes lung function via mechanisms that remain poorly understood. CC chemokine receptor (CCR10) and its ligand CCL28 were both elevated in IPF compared with normal donors. CCR10 was highly expressed by various cells from IPF lungs, most notably stage-specific embryonic antigen-4-positive mesenchymal progenitor cells (MPCs). In vitro, CCL28 promoted the proliferation of CCR10+ MPCs while CRISPR/Cas9-mediated targeting of CCR10 resulted in the death of MPCs. Following the intravenous injection of various cells from IPF lungs into immunodeficient (NOD/SCID-γ, NSG) mice, human CCR10+ cells initiated and maintained fibrosis in NSG mice. Eph receptor A3 (EphA3) was among the highest expressed receptor tyrosine kinases detected on IPF CCR10+ cells. Ifabotuzumab-targeted killing of EphA3+ cells significantly reduced the numbers of CCR10+ cells and ameliorated pulmonary fibrosis in humanized NSG mice. Thus, human CCR10+ cells promote pulmonary fibrosis, and EphA3 mAb-directed elimination of these cells inhibits lung fibrosis.

Indexed as

Alveolar Epithelial CellsAnimalsAntibodies, MonoclonalChemokines, CCCRISPR-Cas SystemsFibroblastsGene Knockout TechniquesHumansIdiopathic Pulmonary FibrosisMesenchymal Stem CellsMiceMice, Inbred NODMice, SCIDReceptor, EphA3Receptors, CCR10Antibodies, MonoclonalCCL28 protein, humanCCR10 protein, humanChemokines, CCEPHA3 protein, humanKB004Receptor, EphA3Receptors, CCR10FibrosisPulmonology

Identifiers

PMID33945505
PMCPMC8262321
OpenAlexW3159911051

What OpenQuestion holds

Textmetadata
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.