Evidence map›Paper›PMID 37781920›Full record

ArticleThe Journal of clinical investigation2023

STING activation promotes autologous type I interferon-dependent development of type 1 regulatory T cells during malaria.

Yulin Wang, Fabian De Labastida Rivera, Chelsea L Edwards, Teija Cm Frame, Jessica A Engel, Luzia Bukali, Jinrui Na, Susanna S Ng, Dillon Corvino, Marcela Montes de Oca and 11 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

21 authors at 5 institutions in 3 countries.

Yulin WangQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Fabian De Labastida RiveraQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Chelsea L EdwardsQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Teija Cm FrameQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jessica A EngelQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Luzia BukaliQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jinrui NaQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Susanna S NgQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Dillon CorvinoQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Marcela Montes de OcaYork Biomedical Research Institute, Hull York Medical School, University of York, York, United Kingdom.
Patrick T BunnQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Megan Sf SoonQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Dean AndrewQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jessica R LoughlandQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jia ZhangQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Fiona H AmanteQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Bridget E BarberQIMR Berghofer Medical Research Institute, Brisbane, Australia.
James S McCarthyVictorian Infectious Diseases Services, Doherty Institute, University of Melbourne, Melbourne, Australia.
J Alejandro LopezQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Michelle J BoyleQIMR Berghofer Medical Research Institute, Brisbane, Australia.
Christian R EngwerdaQIMR Berghofer Medical Research Institute, Brisbane, Australia.
QIMR Berghofer Medical Research Institute · AUThe University of Queensland · AUGriffith University · AUBurnet Institute · AUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of highly effective malaria vaccines and improvement of drug-treatment protocols to boost antiparasitic immunity are critical for malaria elimination. However, the rapid establishment of parasite-specific immune regulatory networks following exposure to malaria parasites hampers these efforts. Here, we identified stimulator of interferon genes (STING) as a critical mediator of type I interferon production by CD4+ T cells during blood-stage Plasmodium falciparum infection. The activation of STING in CD4+ T cells by cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) stimulated IFNB gene transcription, which promoted development of IL-10- and IFN-γ-coproducing CD4+ T (type I regulatory [Tr1]) cells. The critical role for type I IFN signaling for Tr1 cell development was confirmed in vivo using a preclinical malaria model. CD4+ T cell sensitivity to STING phosphorylation was increased in healthy volunteers following P. falciparum infection, particularly in Tr1 cells. These findings identified STING expressed by CD4+ T cells as an important mediator of type I IFN production and Tr1 cell development and activation during malaria.

Indexed as

Interferon Type IMalaria, FalciparumT-Lymphocytes, RegulatoryCD4-Positive T-LymphocytesHumansSTING ProteinInterferon Type ISTING1 protein, humanSTING ProteinCellular immune responseInfectious disease

Identifiers

PMID37781920
PMCPMC10541195
OpenAlexW4387229405

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.