Evidence map›Paper›PMID 23142774›Full record

ArticleNature immunology2013

Neutrophil infiltration during inflammation is regulated by PILRα via modulation of integrin activation.

Jing Wang, Ikuo Shiratori, Junji Uehori, Masahito Ikawa, Hisashi Arase

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  20. A new way to maintain CD8Signal transduction and targeted therapy · 2022
    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

5 authors.

Jing WangDepartment of Immunochemistry, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Ikuo Shiratori
Junji Uehori
Masahito Ikawa
Hisashi Arase

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute inflammatory responses are important in host defense, whereas dysregulated inflammation results in life-threatening complications. Here we found that paired immunoglobulin-like type 2 receptor alpha (PILRα), an inhibitory receptor containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs), negatively regulated neutrophil infiltration during inflammation. Pilra(-/-) mice had increased neutrophil recruitment to inflammatory sites and were highly susceptible to endotoxin shock. Pilra(-/-) neutrophils showed enhanced transmigration ability and increased adhesion to the β(2) integrin ligand ICAM-1. PILRα expressed on neutrophils constitutively associated in cis with its ligands, resulting in clustering of PILRα during stimulation with a chemoattractant. Clustering of PILRα enhanced ITIM-mediated signaling, thus modulating β(2) integrin inside-out activation. These data demonstrate that neutrophil recruitment in inflammatory responses is regulated by PILRα via modulation of integrin activation.

Indexed as

AnimalsCell AdhesionCell MovementCells, CulturedGenetic Predisposition to DiseaseInflammationIntegrinsIntercellular Adhesion Molecule-1MiceMice, KnockoutNeutrophilsN-Formylmethionine Leucyl-PhenylalanineReceptor AggregationReceptors, ImmunologicShock, SepticIntegrinsIntercellular Adhesion Molecule-1N-Formylmethionine Leucyl-PhenylalaninePILRalpha protein, mouseReceptors, Immunologic

Identifiers

PMID23142774

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.