Evidence map›Paper›PMID 42709885›Full record

ArticlePLoS pathogens2026

Exploring the functions of NKG7 in CD4+ and CD8+ T cells during malaria.

Teija C-M Frame, Fabian de Labastida Rivera, Nicholas L Dooley, Jessica A Engel, Jinrui Na, Yulin Wang, Luzia Bukali, Susanna S Ng, Patrick T Bunn, Lynette Beattie and 8 more

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In one paragraph

Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Teija C-M FrameQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Fabian de Labastida RiveraQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Nicholas L DooleyBurnet Institute, Melbourne, Australia.
Jessica A EngelQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jinrui NaQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Yulin WangQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Luzia BukaliQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Susanna S NgUniversity of Bonn, Bonn, Germany.
Patrick T BunnQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Lynette BeattieDepartment of Infectious Diseases, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.
Gunter HartelQIMR Berghofer Medical Research Institute, Brisbane, Australia.ORCID 0000-0002-5454-6450
Timothy WilliamMenzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia.
Matthew J GriggMenzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia.
Nicholas M AnsteyMenzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia.
James S McCarthyDepartment of Infectious Diseases, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.
Bridget E BarberQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Michelle J BoyleBurnet Institute, Melbourne, Australia.
Christian R EngwerdaQIMR Berghofer Medical Research Institute, Brisbane, Australia.ORCID 0000-0003-2813-4804

Funding

Medical Foundation FellowshipNational Health and Medical Research Council of AustraliaSenior Research Fellowship
6 · The paper itself

Abstract

Malaria, caused by Plasmodium parasites, is a significant global health issue. CD4+ and CD8+ T cells are important for immunity against Plasmodium infections, but the specific roles of many immune-related effector molecules in T cells remain poorly defined. Here, we investigated the function of NK cell granule protein 7 (NKG7) in T cells during malaria, focusing on its role in CD4+ and CD8+ T cells in Plasmodium blood-stage responses. In a non-lethal malaria model, NKG7 regulated the development of pro-inflammatory T helper 1 (Th1), IL-10-producing type 1 regulatory (Tr1), and T follicular helper cell responses. In a model of cerebral malaria, NKG7 had a cell-intrinsic role in regulating perforin and granzyme B expression, as well as Tr1 cell development. Human investigations involving peripheral blood mononuclear cells from volunteers participating in controlled human P. falciparum malaria infection studies, as well as endemic country patients with P. falciparum and P. vivax malaria, corroborated these findings. High NKG7 expression in T cells from Plasmodium-infected humans was observed, as well as differences in NKG7 expression based on the infecting Plasmodium species. NKG7 expression was associated with both cytotoxic and non-cytotoxic T cells, indicating varied functions following infection. These results advance our understanding about NKG7's role in T cell-mediated malaria immunity and suggest potential for targeting NKG7 to improve outcomes following Plasmodium infection.

Indexed as

CD4-Positive T-LymphocytesCD8-Positive T-LymphocytesMalariaMalaria, FalciparumMalaria, VivaxAnimalsFemaleHumansMalaria, CerebralMicePlasmodium falciparumPlasmodium vivax

Identifiers

PMID42709885
PMCPMC13568510

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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.