Evidence map›Paper›PMID 32913355›Full record

ArticlePLoS pathogens2020

Contributions of IFN-γ and granulysin to the clearance of Plasmodium yoelii blood stage.

Natália Satchiko Hojo-Souza, Patrick Orestes de Azevedo, Júlia Teixeira de Castro, Andréa Teixeira-Carvalho, Judy Lieberman, Caroline Junqueira, Ricardo Tostes Gazzinelli

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 11% 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, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Characteristics of CD103Frontiers in cellular and infection microbiology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Immunological characteristics of CD103Parasitology research · 2023
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Frontiers in immunology · 2022
    Review
  16. Article
  17. Review
  18. Rodent Malaria Erythrocyte Preference Assessment by anFrontiers in cellular and infection microbiology · 2021
    Article
  19. Article
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

7 authors at 4 institutions in 2 countries.

Natália Satchiko Hojo-SouzaLaboratório de Imunopatologia, Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil.
Patrick Orestes de AzevedoLaboratório de Imunopatologia, Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil.
Júlia Teixeira de CastroLaboratório de Imunopatologia, Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil.ORCID 0000-0003-2620-328X
Andréa Teixeira-CarvalhoGrupo Integrado de Pesquisas em Biomarcadores, Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil.
Judy LiebermanProgram in Cellular and Molecular Medicine, Boston Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA, United States of America.ORCID 0000-0002-6200-4715
Caroline JunqueiraLaboratório de Imunopatologia, Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil.ORCID 0000-0003-0545-0986
Ricardo Tostes GazzinelliLaboratório de Imunopatologia, Instituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, MG, Brazil.ORCID 0000-0003-2427-7699
Fundação Oswaldo Cruz · BRBoston Children's Hospital · USUniversidade Federal de Minas Gerais · BRUniversity of Massachusetts Chan Medical School · US

Funding

Sugar-feeding behavior of the malaria vector Nyssorhynchus darlingi and development of effective attractive toxic sugar baits (ATSB) to increase intervention success in PeruU19AI089681 · NIAID · YALE UNIVERSITY · PI VINETZ, JOSEPH M. · 2010 to 2023
$20.1M
Innate Immune Activation in MalariaR01AI079293 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FITZGERALD, KATHERINE A., GOLENBOCK, DOUGLAS T · 2009 to 2024
$10.9M
UMass Mouse Metabolic Phenotyping Center - Metabolism CoreU2CDK093000 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2016 to 2021
$4.6M
Monocyte-derived dendritic cells in malariaR01NS098747 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GAZZINELLI, RICARDO TOSTES, LUSTER, ANDREW D · 2016 to 2020
$2.1M
Killing of P. vivax infected reticulocytes by cytotoxic T cellsR21AI131632 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GAZZINELLI, RICARDO TOSTES, LIEBERMAN, JUDY · 2018 to 2019
$484k
Host Ciracadian Clock and MalariaR21AI150546 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GAZZINELLI, RICARDO TOSTES · 2020 to 2021
$461k
NIAID NIH HHS R01 AI079293NIAID NIH HHS R21 AI131632NIAID NIH HHS R21 AI150546NIAID NIH HHS U19 AI089681NIDDK NIH HHS U2C DK093000NINDS NIH HHS R01 NS098747
6 · The paper itself

Abstract

P. vivax-infected Retics (iRetics) express human leukocyte antigen class I (HLA-I), are recognized by CD8+ T cells and killed by granulysin (GNLY) and granzymes. However, how Plasmodium infection induces MHC-I expression on Retics is unknown. In addition, whether GNLY helps control Plasmodium infection in vivo has not been studied. Here, we examine these questions using rodent infection with the P. yoelii 17XNL strain, which has tropism for Retics. Infection with P. yoelii caused extramedullary erythropoiesis, reticulocytosis and expansion of CD8+CD44+CD62L- IFN-γ-producing T cells that form immune synapses with iRetics. We now provide evidence that MHC-I expression by iRetic is dependent on IFN-γ-induced transcription of IRF-1, MHC-I and β2-microglobulin (β2-m) in erythroblasts. Consistently, CTLs from infected wild type (WT) mice formed immune synapses with iRetics in an IFN-γ- and MHC-I-dependent manner. When challenged with P. yoelii 17XNL, WT mice cleared parasitemia and survived, while IFN-γ KO mice remained parasitemic and all died. β2-m KO mice that do not express MHC-I and have virtually no CD8+ T cells had prolonged parasitemia, and 80% survived. Because mice do not express GNLY, GNLY-transgenic mice can be used to assess the in vivo importance of GNLY. Parasite clearance was accelerated in GNLY-transgenic mice and depletion of CD8+ T cells ablated the GNLY-mediated resistance to P. yoelii. Altogether, our results indicate that in addition to previously described mechanisms, IFN-γ promotes host resistance to the Retic-tropic P. yoelii 17XNL strain by promoting MHC-I expression on iRetics that become targets for CD8+ cytotoxic T lymphocytes and GNLY.

Indexed as

AnimalsAntigens, Differentiation, T-LymphocyteCD8-Positive T-LymphocytesInterferon-gammaMalariaMiceMice, Inbred BALB CMice, KnockoutPlasmodium yoeliiAntigens, Differentiation, T-LymphocyteGNLY protein, humanIFNG protein, mouseInterferon-gamma

Identifiers

PMID32913355
PMCPMC7482970
OpenAlexW3084836046

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.