Evidence map›Paper›PMID 21171993›Full record

ArticleCritical care (London, England)2010

Common NFKBIL2 polymorphisms and susceptibility to pneumococcal disease: a genetic association study.

Stephen J Chapman, Chiea C Khor, Fredrik O Vannberg, Anna Rautanen, Andrew Walley, Shelley Segal, Catrin E Moore, Robert J O Davies, Nicholas P Day, Norbert Peshu and 5 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. TONSL promotes lung adenocarcinoma progression, immune escape and drug sensitivity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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  5. Review
  6. Article
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  8. Article
  9. Article
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  11. Evolution, revolution and heresy in the genetics of infectious disease susceptibility.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2012
    Review
  12. Review
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

15 authors at 5 institutions in 3 countries.

Stephen J ChapmanThe Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK. schapman@well.ox.ac.uk
Chiea C Khor
Fredrik O Vannberg
Anna Rautanen
Andrew Walley
Shelley Segal
Catrin E Moore
Robert J O Davies
Nicholas P Day
Norbert Peshu
Derrick W Crook
James A Berkley
Thomas N Williams
J Anthony Scott
Adrian V S Hill
University of Oxford · GBKenya Medical Research Institute · KEJohn Radcliffe Hospital · GBCentre for Human Genetics · GBChurchill Hospital · GB

Funding

Wellcome Trust 061089Wellcome Trust 076934Wellcome Trust 081835Wellcome Trust 091758
6 · The paper itself

Abstract

introductionStreptococcus pneumoniae remains a major global health problem and a leading cause of death in children worldwide. The factors that influence development of pneumococcal sepsis remain poorly understood, although increasing evidence points towards a role for genetic variation in the host's immune response. Recent insights from the study of animal models, rare human primary immunodeficiency states, and population-based genetic epidemiology have focused attention on the role of the proinflammatory transcription factor NF-κB in pneumococcal disease pathogenesis. The possible role of genetic variation in the atypical NF-κB inhibitor IκB-R, encoded by NFKBIL2, in susceptibility to invasive pneumococcal disease has not, to our knowledge, previously been reported upon.

methodsAn association study was performed examining the frequencies of nine common NFKBIL2 polymorphisms in two invasive pneumococcal disease case-control groups: European individuals from hospitals in Oxfordshire, UK (275 patients and 733 controls), and African individuals from Kilifi District Hospital, Kenya (687 patients with bacteraemia, of which 173 patients had pneumococcal disease, together with 550 controls).

resultsFive polymorphisms significantly associated with invasive pneumococcal disease susceptibility in the European study, of which two polymorphisms also associated with disease in African individuals. Heterozygosity at these loci was associated with protection from invasive pneumococcal disease (rs760477, Mantel-Haenszel 2 × 2 χ(2) = 11.797, P = 0.0006, odds ratio = 0.67, 95% confidence interval = 0.53 to 0.84; rs4925858, Mantel-Haenszel 2 × 2 χ(2) = 9.104, P = 0.003, odds ratio = 0.70, 95% confidence interval = 0.55 to 0.88). Linkage disequilibrium was more extensive in European individuals than in Kenyans.

conclusionsCommon NFKBIL2 polymorphisms are associated with susceptibility to invasive pneumococcal disease in European and African populations. These findings further highlight the importance of control of NF-κB in host defence against pneumococcal disease.

Indexed as

AdolescentAdultAgedAged, 80 and overCase-Control StudiesChildChild, PreschoolFemaleGenetic Association StudiesGenetic LinkageGenetic Predisposition to DiseaseHumansInfantInfant, NewbornMaleMiddle AgedNF-kappa BTONSL protein, human

Identifiers

PMID21171993
PMCPMC3220025
OpenAlexW2133845337

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.