Evidence map›Paper›PMID 24035192›Full record

ArticleCell2013

Human SNP links differential outcomes in inflammatory and infectious disease to a FOXO3-regulated pathway.

James C Lee, Marion Espéli, Carl A Anderson, Michelle A Linterman, Joanna M Pocock, Naomi J Williams, Rebecca Roberts, Sebastien Viatte, Bo Fu, Norbert Peshu and 15 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 4 pooled it
13.9field-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

124 citing papers in PubMed, 4 syntheses or guidelines pooled it, 229 citations in OpenAlex.

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  18. FOXO3: at the crossroads of metabolic, inflammatory, and tumorigenic remodeling in the colon.American journal of physiology. Gastrointestinal and liver physiology · 2024
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64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 12 institutions in 6 countries.

James C LeeCambridge Institute for Medical Research, University of Cambridge, Cambridge Biomedical Campus, Cambridge CB2 0XY, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Marion Espéli
Carl A Anderson
Michelle A Linterman
Joanna M Pocock
Naomi J Williams
Rebecca Roberts
Sebastien Viatte
Bo Fu
Norbert Peshu
Tran Tinh Hien
Nguyen Hoan Phu
Emma Wesley
Cathryn Edwards
Tariq Ahmad
John C Mansfield
Richard Gearry
Sarah Dunstan
Thomas N Williams
Anne Barton
Carola G Vinuesa
UK IBD Genetics Consortium
Miles Parkes
Paul A Lyons
Kenneth G C Smith
University of Cambridge · GBManchester Academic Health Science Centre · GBAustralian National University · AUKenya Medical Research Institute · KEUniversity of Exeter · GBUniversity of Otago · NZHospital for Tropical Diseases · VNNewcastle University · GBOxford University Clinical Research Unit · VNTorbay Hospital · GBUniversity of Oxford · GBWellcome Sanger Institute · GB

Funding

Arthritis Research UK 20385Chief Scientist Office CZB/4/540Chief Scientist Office ETM/137Chief Scientist Office ETM/75Department of Health NIHR-RP-R3-12-026Medical Research Council G0400929Medical Research Council G0600329Medical Research Council G0800675Medical Research Council G0800759Wellcome Trust 079895Wellcome Trust 083650/Z/07/ZWellcome Trust 087007/Z/08/ZWellcome Trust 089276Wellcome Trust 091758Wellcome Trust 091758/Z/10/ZWellcome Trust 092654Wellcome Trust 098051Wellcome Trust 100140Wellcome Trust 102974
6 · The paper itself

Abstract

The clinical course and eventual outcome, or prognosis, of complex diseases varies enormously between affected individuals. This variability critically determines the impact a disease has on a patient's life but is very poorly understood. Here, we exploit existing genome-wide association study data to gain insight into the role of genetics in prognosis. We identify a noncoding polymorphism in FOXO3A (rs12212067: T > G) at which the minor (G) allele, despite not being associated with disease susceptibility, is associated with a milder course of Crohn's disease and rheumatoid arthritis and with increased risk of severe malaria. Minor allele carriage is shown to limit inflammatory responses in monocytes via a FOXO3-driven pathway, which through TGFβ1 reduces production of proinflammatory cytokines, including TNFα, and increases production of anti-inflammatory cytokines, including IL-10. Thus, we uncover a shared genetic contribution to prognosis in distinct diseases that operates via a FOXO3-driven pathway modulating inflammatory responses.

Indexed as

Polymorphism, Single NucleotideAnimalsArthritis, RheumatoidbetaIG-H3 ProteinCell NucleusCrohn DiseaseExtracellular Matrix ProteinsForkhead Box Protein O3Forkhead Transcription FactorsGenetic VariationHumansInflammationMalaria, FalciparumMiceMonocytesTranscription, GeneticbetaIG-H3 ProteinExtracellular Matrix ProteinsForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanTransforming Growth Factor beta

Identifiers

PMID24035192
PMCPMC3790457
OpenAlexW2110027059

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.