Evidence map›Paper›PMID 2550928›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1989

Reciprocal inhibition of binding between interleukin 3 and granulocyte-macrophage colony-stimulating factor to human eosinophils.

A F Lopez, J M Eglinton, D Gillis, L S Park, S Clark, M A Vadas

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
17.0field-weighted citation impact, top 1% 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, 130 citations in OpenAlex.

  1. Dual Role of GM-CSF as a Pro-Inflammatory and a Regulatory Cytokine: Implications for Immune Therapy.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
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  7. Identification of receptor-binding domains on human interleukin 5 and design of an interleukin 5-derived receptor antagonist.Proceedings of the National Academy of Sciences of the United States of America · 1995
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  13. A human interleukin 3 analog with increased biological and binding activities.Proceedings of the National Academy of Sciences of the United States of America · 1992
    Article
  14. Article
  15. Article
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  18. Eosinophils: a review.Veterinary research communications · 1992
    Review
  19. 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

6 authors at 1 institution in 1 country.

A F LopezDivision of Human Immunology, Institute of Medical and Veterinary Science, Adelaide, South Australia.
J M Eglinton
D Gillis
L S Park
S Clark
M A Vadas
South Australia Pathology · AU

Funding

ROLE OF HUMAN IL-3 IN NORMAL &LEUKEMIC MYELOID CELLSR01CA045822 · NCI · INSTITUTE OF MEDICAL AND VET SCIENCE · PI VADAS, MATHEW · 1987 to 1992
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NCI NIH HHS 1 RO1 CA 45822-01
6 · The paper itself

Abstract

125I-labeled recombinant human interleukin 3 (IL-3) bound, at 4 degrees C, to a single class of high-affinity receptors on human eosinophils with an apparent dissociation constant (Kd) of 470 pM, but it did not bind to human neutrophils. 125I-labeled recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) also bound to a single class of high-affinity receptors on eosinophils with an apparent Kd of 44 pM and on neutrophils with an apparent Kd of 70 pM. These binding characteristics were consistent with the biological activities of IL-3 and GM-CSF on eosinophils and with the lack of stimulation of neutrophil function by IL-3. Specificity studies under conditions shown to prevent receptor internalization showed that the binding of 125I-labeled IL-3 to eosinophils was partially inhibited by GM-CSF but not by other cytokines. Reciprocal experiments with 125I-labeled GM-CSF showed that IL-3 but not other cytokines partially inhibited binding to eosinophils. In contrast, the binding of 125I-labeled GM-CSF to neutrophils was not inhibited by IL-3 or other cytokines tested. Quantitative inhibition binding experiments on eosinophils showed that the reciprocal inhibition between IL-3 and GM-CSF was not complete up to a concentration of heterologous ligand of 100 nM. These results show that (i) IL-3 binds to eosinophils but not neutrophils and (ii) IL-3 and GM-CSF specifically interact on the surface of eosinophils, providing a possible mechanism for the overlapping activities of IL-3 and GM-CSF on these cells.

Indexed as

Antibody-Dependent Cell CytotoxicityColony-Stimulating FactorsEosinophilsGranulocyte-Macrophage Colony-Stimulating FactorGrowth SubstancesHumansInterleukin-3KineticsNeutrophilsReceptors, Antigen, T-CellReceptors, Cell SurfaceReceptors, Colony-Stimulating FactorReceptors, ImmunologicReceptors, Interleukin-3Recombinant ProteinsColony-Stimulating FactorsGranulocyte-Macrophage Colony-Stimulating FactorGrowth SubstancesInterleukin-3Receptors, Antigen, T-CellReceptors, Cell SurfaceReceptors, Colony-Stimulating FactorReceptors, ImmunologicReceptors, Interleukin-3Recombinant Proteins

Identifiers

PMID2550928
PMCPMC297984
OpenAlexW2005150994

What OpenQuestion holds

Textmetadata
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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.