Evidence map›Paper›PMID 28953967›Full record

ArticlePLoS pathogens2017

Malaria-induced interferon-γ drives the expansion of Tbethi atypical memory B cells.

Nyamekye Obeng-Adjei, Silvia Portugal, Prasida Holla, Shanping Li, Haewon Sohn, Abhijit Ambegaonkar, Jeff Skinner, Georgina Bowyer, Ogobara K Doumbo, Boubacar Traore and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

111 citing papers in PubMed, 169 citations in OpenAlex.

  1. Trial
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  4. The Antigen Presenting Potential of CD21Frontiers in immunology · 2020
    Trial
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  6. Trial
  7. Article
  8. Article
  9. Article
  10. Human CD21Journal of human immunity · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. T follicular helper cell development during malaria.Current opinion in immunology · 2025
    Review
  17. Hepatitis C virus modifiedJournal of virology · 2025
    Article
  18. Article
  19. Article
  20. Article

51 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 4 countries.

Nyamekye Obeng-AdjeiMalaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
Silvia PortugalMalaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
Prasida HollaLymphocyte Activation Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.ORCID http://orcid.org/0000-0001-5479-668X
Shanping LiMalaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
Haewon SohnLymphocyte Activation Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
Abhijit AmbegaonkarLymphocyte Activation Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.ORCID http://orcid.org/0000-0001-9778-7396
Jeff SkinnerMalaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.ORCID http://orcid.org/0000-0001-5697-0442
Georgina BowyerThe Jenner Institute Laboratories, University of Oxford, Oxford, United Kingdom.ORCID http://orcid.org/0000-0002-2058-4045
Ogobara K DoumboMalaria Research and Training Centre, Department of Epidemiology of Parasitic Diseases, International Center of Excellence in Research, University of Sciences, Technique and Technology of Bamako, Bamako, Mali.
Boubacar TraoreMalaria Research and Training Centre, Department of Epidemiology of Parasitic Diseases, International Center of Excellence in Research, University of Sciences, Technique and Technology of Bamako, Bamako, Mali.
Susan K PierceLymphocyte Activation Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
Peter D CromptonMalaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.ORCID http://orcid.org/0000-0001-5629-0412
National Institutes of Health · USUniversity of Bamako · MLUniversity of Oxford · GB

Funding

Mechanisms of naturally-acquired immunity to malaria and clinical trials of anti-malaria monoclonal antibodiesZIAAI001155 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CROMPTON, PETER · 2011 to 2025
$30.9M
Mali International Center for Excellence in Research: Malaria immunologyZIAAI001064 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI PIERCE, SUSAN · 2009 to 2025
$25.1M
6 · The paper itself

Abstract

Many chronic infections, including malaria and HIV, are associated with a large expansion of CD21-CD27- 'atypical' memory B cells (MBCs) that exhibit reduced B cell receptor (BCR) signaling and effector functions. Little is known about the conditions or transcriptional regulators driving atypical MBC differentiation. Here we show that atypical MBCs in malaria-exposed individuals highly express the transcription factor T-bet, and that T-bet expression correlates inversely with BCR signaling and skews toward IgG3 class switching. Moreover, a longitudinal analysis of a subset of children suggested a correlation between the incidence of febrile malaria and the expansion of T-bethi B cells. The Th1-cytokine containing supernatants of malaria-stimulated PBMCs plus BCR cross linking induced T-bet expression in naïve B cells that was abrogated by neutralizing IFN-γ or blocking the IFN-γ receptor on B cells. Accordingly, recombinant IFN-γ plus BCR cross-linking drove T-bet expression in peripheral and tonsillar B cells. Consistent with this, Th1-polarized Tfh (Tfh-1) cells more efficiently induced T-bet expression in naïve B cells. These data provide new insight into the mechanisms underlying atypical MBC differentiation.

Indexed as

AdolescentAdultB-LymphocytesBrachyury ProteinCell DifferentiationChildChild, PreschoolFemaleFetal ProteinsGene Expression RegulationHumansImmunologic MemoryInfantInterferon-gammaMalariaMaleBrachyury ProteinFetal ProteinsInterferon-gammaReceptors, Antigen, B-CellT-Box Domain Proteins

Identifiers

PMID28953967
PMCPMC5633206
OpenAlexW2760121721

What OpenQuestion holds

Textmetadata
LicenceCC0
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.