Evidence map›Paper›PMID 24691125›Full record

ArticlePloS one2014

The contribution of natural killer complex loci to the development of experimental cerebral malaria.

Diana S Hansen, Victoria Ryg-Cornejo, Lisa J Ioannidis, Chris Y Chiu, Ann Ly, Catherine Q Nie, Anthony A Scalzo, Louis Schofield

Abstract read
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In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Ion channel mediated mechanotransduction in immune cells.Current opinion in solid state & materials science · 2021
    Article
  2. Review
  3. Review
  4. PeerJ · 2018
    Article
  5. NK Cells: Uncertain Allies against Malaria.Frontiers in immunology · 2017
    Review
  6. Review
  7. Cerebral malaria: gamma-interferon redux.Frontiers in cellular and infection microbiology · 2014
    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

8 authors.

Diana S HansenThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Victoria Ryg-CornejoThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
Lisa J IoannidisThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Chris Y ChiuThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
Ann LyThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Catherine Q NieBurnet Institute, Melbourne, Victoria, Australia.
Anthony A ScalzoCentre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia; Centre for Ophthalmology and Visual Science, The University of Western Australia, Nedlands, Western Australia, Australia.
Louis SchofieldThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Australian Institute of Tropical Health and Medicine, James Cook University, Douglas, Queensland, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Natural Killer Complex (NKC) is a genetic region of highly linked genes encoding several receptors involved in the control of NK cell function. The NKC is highly polymorphic and allelic variability of various NKC loci has been demonstrated in inbred mice, providing evidence for NKC haplotypes. Using BALB.B6-Cmv1r congenic mice, in which NKC genes from C57BL/6 mice were introduced into the BALB/c background, we have previously shown that the NKC is a genetic determinant of malarial pathogenesis. C57BL/6 alleles are associated with increased disease-susceptibility as BALB.B6-Cmv1r congenic mice had increased cerebral pathology and death rates during P. berghei ANKA infection than cerebral malaria-resistant BALB/c controls.

methodsTo investigate which regions of the NKC are involved in susceptibility to experimental cerebral malaria (ECM), intra-NKC congenic mice generated by backcrossing recombinant F2 progeny from a (BALB/c x BALB.B6-Cmv1r) F1 intercross to BALB/c mice were infected with P. berghei ANKA.

resultsOur results revealed that C57BL/6 alleles at two locations in the NKC contribute to the development of ECM. The increased severity to severe disease in intra-NKC congenic mice was not associated with higher parasite burdens but correlated with a significantly enhanced systemic IFN-γ response to infection and an increased recruitment of CD8+ T cells to the brain of infected animals.

conclusionsPolymorphisms within the NKC modulate malarial pathogenesis and acquired immune responses to infection.

Indexed as

Genetic LociAllelesAnimalsBiomarkersDisease Models, AnimalGene Expression RegulationGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeInterferon-gammaKiller Cells, NaturalLectins, C-TypeMalaria, CerebralMiceMice, Inbred C57BLNatural Killer T-CellsBiomarkersClec4n protein, mouseInterferon-gammaLectins, C-TypeReceptors, Cell Surface

Identifiers

PMID24691125
PMCPMC3972225

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LicenceCC BY
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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.