Evidence map›Paper›PMID 26667315›Full record

Trial reportThe Journal of infectious diseases2016

Frequent Malaria Drives Progressive Vδ2 T-Cell Loss, Dysfunction, and CD16 Up-regulation During Early Childhood.

Lila A Farrington, Prasanna Jagannathan, Tara I McIntyre, Hilary M Vance, Katherine Bowen, Michelle J Boyle, Felistas Nankya, Samuel Wamala, Ann Auma, Mayimuna Nalubega and 7 more

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in The Journal of infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  3. Review
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  13. Article
  14. Article
  15. RepeatedScience translational medicine · 2021
    Article
  16. Review
  17. Article
  18. γδ T cells burst malaria's bubble.Nature immunology · 2021
    Article
  19. Article
  20. 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

17 authors at 3 institutions in 3 countries.

Lila A FarringtonDepartments of Medicine, University of California San Francisco.
Prasanna JagannathanDepartments of Medicine, University of California San Francisco.
Tara I McIntyreDepartments of Medicine, University of California San Francisco.
Hilary M VanceDepartments of Medicine, University of California San Francisco.
Katherine BowenDepartments of Medicine, University of California San Francisco.
Michelle J BoyleDepartments of Medicine, University of California San Francisco Center for Biomedical Research, The Burnet Institute, Melbourne, Victoria, Australia.
Felistas NankyaInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Samuel WamalaInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Ann AumaInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Mayimuna NalubegaInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Esther SikyomuInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Kate NaluwuInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Victor BigiraInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
James KapisiInfectious Diseases Research Collaboration, Makerere University College of Health Sciences, Kampala, Uganda.
Grant DorseyDepartments of Medicine, University of California San Francisco.
Moses R KamyaDepartment of Medicine, Makerere University College of Health Sciences, Kampala, Uganda.
Margaret E FeeneyDepartments of Medicine, University of California San Francisco Pediatrics, University of California San Francisco.
University of California, San Francisco · USInfectious Diseases Research Collaboration · UGMakerere University · UG

Funding

Transmission ProjectU19AI089674 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHEW G DORSEY, MOSES Robert KAMYA · 2010 to 2026
$29.3M
The immunologic consequences of prenatal exposure to malariaP01HD059454 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DORSEY, MATTHEW G · 2008 to 2017
$22.6M
The role of γδ T cells in fetal and infant immune defense against malariaR01AI093615 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FEENEY, MARGARET E · 2011 to 2025
$9.1M
Mentoring Translational Researchers for Careers in Pediatric Global HealthK24AI113002 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FEENEY, MARGARET E · 2014 to 2023
$1.9M
Immunologic Consequences of Highly Effective Antimalarial ChemopreventionK23AI100949 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAGANNATHAN, PRASANNA · 2012 to 2016
$657k
NIAID NIH HHS K23 AI100949NIAID NIH HHS K24 AI113002NIAID NIH HHS K24AI113002NIAID NIH HHS R01 AI093615NIAID NIH HHS R01AI093615NIAID NIH HHS U19 AI089674NICHD NIH HHS P01 HD059454NICHD NIH HHS P01 HD059454-03
6 · The paper itself

Abstract

γδ T cells expressing Vδ2 may be instrumental in the control of malaria, because they inhibit the replication of blood-stage parasites in vitro and expand during acute malaria infection. However, Vδ2 T-cell frequencies and function are lower among children with heavy prior malaria exposure. It remains unclear whether malaria itself is driving this loss. Here we measure Vδ2 T-cell frequency, cytokine production, and degranulation longitudinally in Ugandan children enrolled in a malaria chemoprevention trial from 6 to 36 months of age. We observed a progressive attenuation of the Vδ2 response only among children incurring high rates of malaria. Unresponsive Vδ2 T cells were marked by expression of CD16, which was elevated in the setting of high malaria transmission. Moreover, chemoprevention during early childhood prevented the development of dysfunctional Vδ2 T cells. These observations provide insight into the role of Vδ2 T cells in the immune response to chronic malaria.

Indexed as

ArtemisininsChild, PreschoolDrug CombinationsGPI-Linked ProteinsHumansImmune ToleranceInfantLongitudinal StudiesMalaria, FalciparumPiperazinesPlasmodium falciparumPyrimethamineQuinolinesReceptors, Antigen, T-Cell, gamma-deltaReceptors, IgGSulfadoxineArtemisininsartenimolDrug Combinationsfanasil, pyrimethamine drug combinationFCGR3B protein, humanGPI-Linked ProteinspiperaquinePiperazinesPyrimethamineQuinolinesReceptors, Antigen, T-Cell, gamma-deltaReceptors, IgGSulfadoxineCD16immunologic tolerancemalariaPlasmodium falciparumγδ T cells

Identifiers

PMID26667315
PMCPMC4813738
OpenAlexW2213031021

What OpenQuestion holds

Textmetadata
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.