Evidence map›Paper›PMID 24133137›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Exocytosis acts as a modulator of the ILT4-mediated inhibition of neutrophil functions.

Jeremy Baudhuin, Julie Migraine, Valerie Faivre, Laure Loumagne, Anne-Claire Lukaszewicz, Didier Payen, Benoit Favier

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

58 citing papers in PubMed, 95 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Jeremy BaudhuinCommissariat à l'Énergie Atomique et aux Énergies Alternatives, Institute of Emerging Diseases and Innovative Therapies, Service de Recherches en Hemato-Immunologie, Hopital St. Louis, 75475 Paris Cedex 10, France.
Julie Migraine
Valerie Faivre
Laure Loumagne
Anne-Claire Lukaszewicz
Didier Payen
Benoit Favier
Sorbonne Paris Cité · FRUniversité Paris Cité · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils play a major role in inflammatory responses and immune defense against pathogens. Even though expression of inhibitory receptors has been reported on neutrophils, their role remains poorly defined. Here we show that primary human neutrophils expressed immunoglobulin-like transcript 4 (ILT4) inhibitory receptor and that this expression was induced during differentiation of the myelomonoblast PLB-985 cell line into "neutrophil-like" cells. Functional assays indicated that human leukocyte antigen G, the preferred ligand of ILT4, inhibited the phagocytic function of neutrophils. ILT4 engagement also impaired reactive oxygen species production induced through CD32a and both receptors were found colocalized into neutrophil lipid rafts. Moreover, neutrophil degranulation induced through inflammatory stimuli increased ILT4 expression as a result of the rapid translocation of an intracellular pool to the cell surface. Consequently to this ILT4 up-regulation, the human leukocyte antigen G-mediated inhibition of neutrophil phagocytic function was enhanced. Finally, we found that ILT4 up-regulation induced on healthy donor neutrophils following stimulation was impaired in presence of plasma from patients with sepsis. Similarly, ILT4 up-regulation was inhibited in neutrophils from septic patients. Altogether, our results reveal a unique mechanism of regulation of neutrophil functions through ILT4 and its exocytosis that may have implications in inflammatory disorders.

Indexed as

ApoptosisExocytosisFlow CytometryGene Expression RegulationHumansMembrane GlycoproteinsMicroscopy, ConfocalNeutrophilsPhagocytosisReactive Oxygen SpeciesReceptors, ImmunologicRespiratory BurstSepsisLILRB2 protein, humanMembrane GlycoproteinsReactive Oxygen SpeciesReceptors, ImmunologicgranulocytesHLA-GinflammationLILRB2

Identifiers

PMID24133137
PMCPMC3816409
OpenAlexW2043731481

What OpenQuestion holds

Textmetadata
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.