Evidence map›Paper›PMID 21818580›Full record

ArticleHuman genetics2012

Functional haplotypes of Fc gamma (Fcγ) receptor (FcγRIIA and FcγRIIIB) predict risk to repeated episodes of severe malarial anemia and mortality in Kenyan children.

Collins Ouma, Gregory C Davenport, Steven Garcia, Prakasha Kempaiah, Ateefa Chaudhary, Tom Were, Samuel B Anyona, Evans Raballah, Stephen N Konah, James B Hittner and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Human genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  5. Susceptibility toFrontiers in immunology · 2020
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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

13 authors at 5 institutions in 2 countries.

Collins OumaCentre for Global Health Research, Kenya Medical Research Institute, University of New Mexico/KEMRI Laboratories of Parasitic and Viral Diseases, Kisumu, Kenya.
Gregory C Davenport
Steven Garcia
Prakasha Kempaiah
Ateefa Chaudhary
Tom Were
Samuel B Anyona
Evans Raballah
Stephen N Konah
James B Hittner
John M Vulule
John M Ong'echa
Douglas J Perkins
Kenya Medical Research Institute · KEUniversity of New Mexico · USCenter for Global Health · USCollege of Charleston · USKenyatta University · KE

Funding

TRAINING AND RESEARCH ON SEVERE MALARIAL ANEMIAD43TW005884 · FIC · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Collins Ouma, Douglas Jay Perkins · 2002 to 2026
$5.2M
Biology of Infectious Diseases &InflammationT32AI007538 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Michelle A Ozbun · 1998 to 2026
$5.2M
GENETIC BASIS OF SEVERE MALARIAL ANEMIAR01AI051305 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PERKINS, DOUGLAS JAY · 2002 to 2011
$4.7M
Impacts of surface receptors [Toll like receptor (TLRs) and Fc gamma receptors (FR01TW008306 · FIC · MASENO UNIVERSITY · PI OUMA, COLLINS · 2009 to 2012
$202k
FIC NIH HHS D43 TW005884FIC NIH HHS R01 TW008306FIC NIH HHS TW008306-02FIC NIH HHS TW05884-02NIAID NIH HHS AI51305-02NIAID NIH HHS R01 AI051305NIAID NIH HHS T32 AI007538
6 · The paper itself

Abstract

Development of protective immunity against Plasmodium falciparum is partially mediated through binding of malaria-specific IgG to Fc gamma (γ) receptors. Variations in human FcγRIIA-H/R-131 and FcγRIIIB-NA1/NA2 affect differential binding of IgG sub-classes. Since variability in FcγR may play an important role in severe malarial anemia (SMA) pathogenesis by mediating phagocytosis of red blood cells and triggering cytokine production, the relationship between FcγRIIA-H/R131 and FcγRIIIB-NA1/NA2 haplotypes and susceptibility to SMA (Hb < 6.0 g/dL) was investigated in Kenyan children (n = 528) with acute malaria residing in a holoendemic P. falciparum transmission region. In addition, the association between carriage of the haplotypes and repeated episodes of SMA and all-cause mortality were investigated over a 3-year follow-up period. Since variability in FcγR can alter interferon (IFN)-γ production, a mediator of innate and adaptive immune responses, functional associations between the haplotypes and IFN-γ were also explored. During acute malaria, children with SMA had elevated peripheral IFN-γ levels (P = 0.006). Although multivariate logistic regression analyses (controlling for covariates) revealed no associations between the FcγR haplotypes and susceptibility to SMA during acute infection, the FcγRIIA-131H/FcγRIIIB-NA1 haplotype was associated with decreased peripheral IFN-γ (P = 0.046). Longitudinal analyses showed that carriage of the FcγRIIA-131H/FcγRIIIB-NA1 haplotype was associated with reduced risk of SMA (RR 0.65, 95% CI 0.46-0.90; P = 0.012) and all-cause mortality (P = 0.002). In contrast, carriers of the FcγRIIA-131H/FcγRIIIB-NA2 haplotype had increased susceptibility to SMA (RR 1.47, 95% CI 1.06-2.04; P = 0.020). Results here demonstrate that variation in the FcγR gene alters susceptibility to repeated episodes of SMA and mortality, as well as functional changes in IFN-γ production.

Indexed as

AnemiaChild, PreschoolGenetic Predisposition to DiseaseGPI-Linked ProteinsHaplotypesHumansInfantInfant, NewbornInterferon-gammaKenyaLongitudinal StudiesMalariaReceptors, IgGRecurrenceFc gamma receptor IIAFCGR3B protein, humanGPI-Linked ProteinsInterferon-gammaReceptors, IgG

Identifiers

PMID21818580
PMCPMC3258363
OpenAlexW1992628453

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Registered trials

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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.