Evidence map›Paper›PMID 28737175›Full record

ArticleNature communications2017

Natural variation of macrophage activation as disease-relevant phenotype predictive of inflammation and cancer survival.

Konrad Buscher, Erik Ehinger, Pritha Gupta, Akula Bala Pramod, Dennis Wolf, George Tweet, Calvin Pan, Charles D Mills, Aldons J Lusis, Klaus Ley

Open access · goldAbstract readComparative Study
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

80 citing papers in PubMed, 121 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Konrad BuscherDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
Erik EhingerDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
Pritha GuptaDepartments of Medicine, Human Genetics, and Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California 90095, USA.
Akula Bala PramodDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
Dennis WolfDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
George TweetDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
Calvin PanDepartments of Medicine, Human Genetics, and Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California 90095, USA.
Charles D MillsBioMedical Consultants, Marine on St. Croix, Minnesota 55047, USA.
Aldons J LusisDepartments of Medicine, Human Genetics, and Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California 90095, USA.
Klaus LeyDivision of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
La Jolla Institute for Immunology · USUniversity of California, Los Angeles · US

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REUE, KAREN · 1985 to 2019
$50.2M
Myeloid cell interactions with T cells in atherosclerosisR01HL115232 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI LEY, KLAUS F. · 2012 to 2018
$3.2M
NHLBI NIH HHS P01 HL028481NHLBI NIH HHS P01 HL030568NHLBI NIH HHS R01 HL115232
6 · The paper itself

Abstract

Although mouse models exist for many immune-based diseases, the clinical translation remains challenging. Most basic and translational studies utilize only a single inbred mouse strain. However, basal and diseased immune states in humans show vast inter-individual variability. Here, focusing on macrophage responses to lipopolysaccharide (LPS), we use the hybrid mouse diversity panel (HMDP) of 83 inbred strains as a surrogate for human natural immune variation. Since conventional bioinformatics fail to analyse a population spectrum, we highlight how gene signatures for LPS responsiveness can be derived based on an Interleukin-12β and arginase expression ratio. Compared to published signatures, these gene markers are more robust to identify susceptibility or resilience to several macrophage-related disorders in humans, including survival prediction across many tumours. This study highlights natural activation diversity as a disease-relevant dimension in macrophage biology, and suggests the HMDP as a viable tool to increase translatability of mouse data to clinical settings.

Indexed as

Genetic VariationModels, AnimalAnimalsGenetic Predisposition to DiseaseHumansImmunity, InnateInflammationLipopolysaccharidesMacrophage ActivationMaleMiceNeoplasmsPhenotypeLipopolysaccharides

Identifiers

PMID28737175
PMCPMC5527282
OpenAlexW2737849140

What OpenQuestion 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 OpenQuestion graph.