Evidence map›Paper›PMID 32477348›Full record

ReviewFrontiers in immunology2020

Leukocyte Immunoglobulin-Like Receptors (LILRs) on Human Neutrophils: Modulators of Infection and Immunity.

Alexander L Lewis Marffy, Alex J McCarthy

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  9. NK Cells: A Powerful Squad Versus SARS-CoV-2.International journal of molecular sciences · 2025
    Review
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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

2 authors at 1 institution in 1 country.

Alexander L Lewis MarffyMRC Centre for Molecular Bacteriology and Infection, Imperial College London, London, United Kingdom.
Alex J McCarthyMRC Centre for Molecular Bacteriology and Infection, Imperial College London, London, United Kingdom.
Imperial College London · GB

Funding

Medical Research Council MR/P028225/1
6 · The paper itself

Abstract

Neutrophils have a crucial role in defense against microbes. Immune receptors allow neutrophils to sense their environment, with many receptors functioning to recognize signs of infection and to promote antimicrobial effector functions. However, the neutrophil response must be tightly regulated to prevent excessive inflammation and tissue damage, and regulation is achieved by expression of inhibitory receptors that can raise activation thresholds. The leukocyte immunoglobulin-like receptor (LILR) family contain activating and inhibitory members that can up- or down-regulate immune cell activity. New ligands and functions for LILR continue to emerge. Understanding the role of LILR in neutrophil biology is of general interest as they can activate and suppress antimicrobial responses of neutrophils and because several human pathogens exploit these receptors for immune evasion. This review focuses on the role of LILR in neutrophil biology. We focus on the current knowledge of LILR expression on neutrophils, the known functions of LILR on neutrophils, and how these receptors may contribute to shaping neutrophil responses during infection.

Indexed as

Antigens, CDHumansImmunity, InnateImmunomodulationInfectionsMembrane GlycoproteinsNeutrophilsReceptors, ImmunologicAntigens, CDLILRA2 protein, humanLILRB2 protein, humanLILRB3 protein, humanMembrane GlycoproteinsReceptors, Immunologicimmune receptorinhibitory receptorinnate immunityLILRLILRA2LILRB2LILRB3neutrophil

Identifiers

PMID32477348
PMCPMC7237751
OpenAlexW3025179027

What Socratic 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 Socratic graph.