ArticleInfection and immunity2015
Phosphoantigen Burst upon Plasmodium falciparum Schizont Rupture Can Distantly Activate Vγ9Vδ2 T Cells.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
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.
Who cites it
26 citing papers in PubMed.
- Longitudinal analysis of gamma delta T cell subsets during malaria infections in Malian adults.Malaria journal · 2019Trial
- γδ T Cells Are Required for the Induction of Sterile Immunity during Irradiated Sporozoite Vaccinations.Journal of immunology (Baltimore, Md. : 1950) · 2017Trial
- Frequent Malaria Drives Progressive Vδ2 T-Cell Loss, Dysfunction, and CD16 Up-regulation During Early Childhood.The Journal of infectious diseases · 2016Trial
- Characterization and anti-tuberculosis effects of γδ T cells expanded and activated byVirulence · 2025Review
- The early human interferon gamma response to Toxoplasma gondii is driven by Vγ9Vδ2 T-cell sensing of host phosphoantigens and subsequent NK-cell activation.PLoS pathogens · 2025Article
- Repeat controlled human Plasmodium falciparum infections delay bloodstream patency and reduce symptoms.Nature communications · 2024Article
- Phenotypic changes of γδ T cells inFrontiers in immunology · 2024Article
- Escaping the enemy's bullets: an update on how malaria parasites evade host immune response.Parasitology research · 2023Review
- γδ T cells as immunotherapy for malaria: balancing challenges and opportunities.Frontiers in immunology · 2023Article
- Review
- γδ T cells burst malaria's bubble.Nature immunology · 2021Article
- γδ T cells suppress Plasmodium falciparum blood-stage infection by direct killing and phagocytosis.Nature immunology · 2021Article
- Immuno-antibiotics: targeting microbial metabolic pathways sensed by unconventional T cells.Immunotherapy advances · 2021Review
- Review
- Opsonized antigen activates Vδ2+ T cells via CD16/FCγRIIIa in individuals with chronic malaria exposure.PLoS pathogens · 2020Article
- Human unconventional T cells in Plasmodium falciparum infection.Seminars in immunopathology · 2020Review
- γδ T Cells KillJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Transcriptional Memory-Like Imprints and Enhanced Functional Activity in γδ T Cells Following Resolution of Malaria Infection.Frontiers in immunology · 2020Article
- γδ-T cells promote IFN-γ-dependentProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Prediction of Disordered Regions and Their Roles in the Anti-Pathogenic and Immunomodulatory Functions of Butyrophilins.Molecules (Basel, Switzerland) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Malaria induces potent activation and expansion of the Vγ9Vδ2 subpopulation of γδT cells, which inhibit the Plasmodium falciparum blood cycle through soluble cytotoxic mediators, abrogating merozoite invasion capacity. Intraerythrocytic stages efficiently trigger Vγ9Vδ2 T-cell activation and degranulation through poorly understood mechanisms. P. falciparum blood-stage extracts are known to contain phosphoantigens able to stimulate Vγ9Vδ2 T cells, but how these are presented by intact infected red blood cells (iRBCs) remains elusive. Here we show that, unlike activation by phosphoantigen-expressing cells, Vγ9Vδ2 T-cell activation by intact iRBCs is independent of butyrophilin expression by the iRBC, and contact with an intact iRBC is not required. Moreover, blood-stage culture supernatants proved to be as potent activators of Vγ9Vδ2 T cells as iRBCs. Bioactivity in the microenvironment is attributable to phosphoantigens, as it is dependent on the parasite DOXP pathway, on Vγ9Vδ2 TCR signaling, and on butyrophilin expression by Vγ9Vδ2 T cells. Kinetic studies showed that the phosphoantigens were released at the end of the intraerythrocytic cycle at the time of parasite egress. We document exquisite sensitivity of Vγ9Vδ2 T cells, which respond to a few thousand parasites. These data unravel a novel framework, whereby release of phosphoantigens into the extracellular milieu by sequestered parasites likely promotes activation of distant Vγ9Vδ2 T cells that in turn exert remote antiparasitic functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.