Evidence map›Paper›PMID 33085728›Full record

ArticlePLoS pathogens2020

Opsonized antigen activates Vδ2+ T cells via CD16/FCγRIIIa in individuals with chronic malaria exposure.

Lila A Farrington, Perri C Callaway, Hilary M Vance, Kayla Baskevitch, Emma Lutz, Lakshmi Warrier, Tara I McIntyre, Rachel Budker, Prasanna Jagannathan, Felistas Nankya and 8 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  10. Natural killer cell antibody-dependent cellular cytotoxicity toClinical & translational immunology · 2024
    Article
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  15. Article
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  17. RepeatedScience translational medicine · 2021
    Article
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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

18 authors at 3 institutions in 2 countries.

Lila A FarringtonDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Perri C CallawayDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Hilary M VanceDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Kayla BaskevitchDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.ORCID 0000-0002-6860-7891
Emma LutzDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Lakshmi WarrierDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Tara I McIntyreDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.ORCID 0000-0001-6670-9977
Rachel BudkerDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.ORCID 0000-0003-4996-9130
Prasanna JagannathanDepartment of Medicine, Stanford University, Stanford, California, United States of America.ORCID 0000-0001-6305-758X
Felistas NankyaInfectious Diseases Research Collaboration, Kampala, Uganda.
Kenneth MusinguziInfectious Diseases Research Collaboration, Kampala, Uganda.
Mayimuna NalubegaInfectious Diseases Research Collaboration, Kampala, Uganda.
Ester SikyomuInfectious Diseases Research Collaboration, Kampala, Uganda.
Kate NaluwuInfectious Diseases Research Collaboration, Kampala, Uganda.
Emmanuel ArinaitweInfectious Diseases Research Collaboration, Kampala, Uganda.
Grant DorseyDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.
Moses R KamyaInfectious Diseases Research Collaboration, Kampala, Uganda.
Margaret E FeeneyDepartment of Medicine, University of California San Francisco, San Francisco, California, United States of America.ORCID 0000-0002-2515-2989
University of California, San Francisco · USInfectious Diseases Research Collaboration · UGStanford University · US

Funding

Clinical and Translational Science InstituteUL1TR001872 · NCATS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI COLLARD, HAROLD R, JACOBY, VANESSA · 2016 to 2025
$112.1M
Transmission ProjectU19AI089674 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHEW G DORSEY, MOSES Robert KAMYA · 2010 to 2026
$29.3M
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
NCATS NIH HHS UL1 TR001872NIAID NIH HHS K24 AI113002NIAID NIH HHS R01 AI093615NIAID NIH HHS U19 AI089674
6 · The paper itself

Abstract

Vγ9Vδ2 T cells rapidly respond to phosphoantigens produced by Plasmodium falciparum in an innate-like manner, without prior antigen exposure or processing. Vδ2 T cells have been shown to inhibit parasite replication in vitro and are associated with protection from P. falciparum parasitemia in vivo. Although a marked expansion of Vδ2 T cells is seen after acute malaria infection in naïve individuals, repeated malaria causes Vδ2 T cells to decline both in frequency and in malaria-responsiveness, and to exhibit numerous transcriptional and phenotypic changes, including upregulation of the Fc receptor CD16. Here we investigate the functional role of CD16 on Vδ2 T cells in the immune response to malaria. We show that CD16+ Vδ2 T cells possess more cytolytic potential than their CD16- counterparts, and bear many of the hallmarks of mature NK cells, including KIR expression. Furthermore, we demonstrate that Vδ2 T cells from heavily malaria-exposed individuals are able to respond to opsonized P.falciparum-infected red blood cells through CD16, representing a second, distinct pathway by which Vδ2 T cells may contribute to anti-parasite effector functions. This response was independent of TCR engagement, as demonstrated by blockade of the phosphoantigen presenting molecule Butyrophilin 3A1. Together these results indicate that Vδ2 T cells in heavily malaria-exposed individuals retain the capacity for antimalarial effector function, and demonstrate their activation by opsonized parasite antigen. This represents a new role both for Vδ2 T cells and for opsonizing antibodies in parasite clearance, emphasizing cooperation between the cellular and humoral arms of the immune system.

Indexed as

AdultChildChild, PreschoolFemaleGPI-Linked ProteinsHumansImmunityInfantMalariaMalaria, FalciparumMaleMiddle AgedParasitemiaPlasmodium falciparumReceptors, IgGT-LymphocytesFCGR3A protein, humanFCGR3B protein, humanGPI-Linked ProteinsReceptors, IgG

Identifiers

PMID33085728
PMCPMC7605717
OpenAlexW3094055182

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.