Evidence map›Paper›PMID 24530099›Full record

Trial reportThe Journal of allergy and clinical immunology2014

The eosinophil surface receptor epidermal growth factor-like module containing mucin-like hormone receptor 1 (EMR1): a novel therapeutic target for eosinophilic disorders.

Fanny Legrand, Nenad Tomasevic, Olga Simakova, Chyi-Chia Richard Lee, Zengfang Wang, Mark Raffeld, Michelle A Makiya, Varghese Palath, John Leung, Mark Baer and 4 more

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  5. Article
  6. Engineering antibody-drug conjugates targeting an adhesion GPCR, CD97.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Emerging Evidence for Pleiotropism of Eosinophils.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

14 authors at 3 institutions in 2 countries.

Fanny LegrandEosinophil Pathology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Md. Electronic address: legrandfa@niaid.nih.gov.
Nenad TomasevicKaloBios Pharmaceuticals, South San Francisco, Calif.
Olga SimakovaHematology Section, Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Md.
Chyi-Chia Richard LeeLaboratory of Pathology, National Cancer Institute, Bethesda, Md.
Zengfang WangLaboratory of Pathology, National Cancer Institute, Bethesda, Md.
Mark RaffeldLaboratory of Pathology, National Cancer Institute, Bethesda, Md.
Michelle A MakiyaEosinophil Pathology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Md.
Varghese PalathKaloBios Pharmaceuticals, South San Francisco, Calif.
John LeungKaloBios Pharmaceuticals, South San Francisco, Calif.
Mark BaerKaloBios Pharmaceuticals, South San Francisco, Calif.
Geoffrey YarrantonKaloBios Pharmaceuticals, South San Francisco, Calif.
Irina MaricHematology Section, Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Md.
Christopher BebbingtonKaloBios Pharmaceuticals, South San Francisco, Calif.
Amy D KlionEosinophil Pathology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Md.
National Cancer Institute · USNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Eosinophils and Eosinophil Activation in the Pathogenesis of Human DiseaseZIAAI001130 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KLION, AMY · 2010 to 2025
$22.5M
Immunohistochemistry Core LaboratoryZICBC011087 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RAFFELD, MARK · 2009 to 2015
$7.4M
Laboratory Assessment of Patients with Hypereosinophilic SyndromeZIACL080004 · CLC · CLINICAL CENTER · PI MARIC, IRINA · 2009 to 2025
$0k
Intramural NIH HHS ZIA AI001130
6 · The paper itself

Abstract

backgroundAlthough several novel agents are currently in clinical trials for eosinophilic disorders, none has demonstrated efficacy in reducing blood and tissue eosinophilia in all subjects. Additional approaches are clearly needed.

objectiveWe sought to explore the potential of the human eosinophil surface receptor epidermal growth factor-like module containing mucin-like hormone receptor 1 (EMR1) as a therapeutic target for eosinophilic disorders.

methodsEMR1 expression was assessed in blood and bone marrow specimens from eosinophilic and healthy subjects, cell lines, CD34(+) cells differentiated in vitro, and tissue biopsy specimens by using flow cytometry, quantitative PCR, and immunostaining. Eosinophil targeting by a novel, humanized, afucosylated anti-EMR1 IgG1 was evaluated in vitro by using a natural killer cell-mediated killing assay and in vivo in cynomolgus monkeys.

resultsAnalysis of blood and bone marrow cells from healthy and eosinophilic donors and in vitro-differentiated CD34(+) cells confirmed restriction of human EMR1 surface and mRNA expression to mature eosinophils. Tissue eosinophils also expressed EMR1. Although EMR1 was highly expressed on eosinophils from all subjects, surface expression was negatively correlated with absolute eosinophil counts (r = -0.46, P < .001), and soluble plasma levels correlated positively with absolute eosinophil counts (r = 0.69, P < .001), suggesting modulation of EMR1 in vivo. Nevertheless, afucosylated anti-EMR1 mAb dramatically enhanced natural killer cell-mediated killing of eosinophils from healthy and eosinophilic donors and induced a rapid and sustained depletion of eosinophils in monkeys.

conclusionEMR1 expression is restricted to mature blood and tissue eosinophils. Targeting of eosinophils with afucosylated anti-EMR1 antibody shows promise as a treatment for eosinophilic disorders.

Indexed as

Antibodies, Monoclonal, Murine-DerivedBone Marrow CellsCalcium-Binding ProteinsCD4-Positive T-LymphocytesEosinophiliaEosinophilsFemaleGene Expression RegulationHumansImmunoglobulin GK562 CellsMaleMembrane GlycoproteinsMucinsReceptors, G-Protein-CoupledU937 CellsADGRE1 protein, humanAntibodies, Monoclonal, Murine-DerivedCalcium-Binding ProteinsImmunoglobulin GMembrane GlycoproteinsMucinsReceptors, G-Protein-Coupledafucosylated antibodyeosinophileosinophiliaEpidermal growth factor–like module containing mucin-like hormone receptor 1hypereosinophilic syndromemAb therapy

Identifiers

PMID24530099
PMCPMC4113341
OpenAlexW2071380169

What OpenQuestion holds

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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.