ArticleInfection and immunity2013
Donor CD8+ T cells prevent Toxoplasma gondii de-encystation but fail to rescue the exhausted endogenous CD8+ T cell population.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Systematic review and meta-analysis of variation in Toxoplasma gondii cyst burden in the murine model.Experimental parasitology · 2019Pooled it
- Clostridium butyricum ameliorates Toxoplasma gondii-induced neuropsychiatric disorders by attenuating glial-mediated synaptic pruning via the gut-brain axis.Journal of neuroinflammation · 2026Article
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- Effects ofFood and waterborne parasitology · 2023Article
- A Lower Dose of Infection Generates a Better Long-Term Immune Response against Toxoplasma gondii.ImmunoHorizons · 2023Article
- Association of gestational diabetes mellitus and negative modulation of the specific humoral and cellular immune response againstFrontiers in immunology · 2022Article
- Genetic mapping reveals Nfkbid as a central regulator of humoral immunity to Toxoplasma gondii.PLoS pathogens · 2021Article
- Optimizing Pyrazolopyrimidine Inhibitors of Calcium Dependent Protein Kinase 1 for Treatment of Acute and Chronic Toxoplasmosis.Journal of medicinal chemistry · 2020Article
- NK Cells Negatively Regulate CD8 T Cells to Promote Immune Exhaustion and ChronicFrontiers in cellular and infection microbiology · 2020Article
- Robust Control of a Brain-Persisting Parasite through MHC I Presentation by Infected Neurons.Cell reports · 2019Article
- Treatment of toxoplasmosis: Current options and future perspectives.Food and waterborne parasitology · 2019Review
- Toxoplasma: Immunity and Pathogenesis.Current clinical microbiology reports · 2019Article
- An Animal Model of Acute and Chronic Chagas Disease With the Reticulotropic Y Strain ofFrontiers in immunology · 2019Article
- PD-L1, TIM-3, and CTLA-4 Blockade Fails To Promote Resistance to Secondary Infection with Virulent Strains of Toxoplasma gondii.Infection and immunity · 2018Article
- Brains and Brawn: Toxoplasma Infections of the Central Nervous System and Skeletal Muscle.Trends in parasitology · 2017Review
- Blimp-1-mediated CD4 T cell exhaustion causes CD8 T cell dysfunction during chronic toxoplasmosis.The Journal of experimental medicine · 2016Article
- CD8+ T cell immunity in an encephalitis model of Toxoplasma gondii infection.Seminars in immunopathology · 2015Review
- Characteristics and critical function of CD8+ T cells in the Toxoplasma-infected brain.Seminars in immunopathology · 2015Review
- Recent advances in Toxoplasma gondii immunotherapeutics.The Korean journal of parasitology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Functional exhaustion of CD8(+) T cells due to increased expression of inhibitory molecule PD-1 (Programmed Death-1) causes reactivation of latent disease during later phases of chronic toxoplasmosis. Onset of disease recrudescence results in decreased parasite cyst burden concomitant with parasites undergoing stage conversion from a primarily encysted, quiescent bradyzoite to a fast-replicating, highly motile tachyzoite. Thus, reduced cyst burden is one of the early hallmarks of disease recrudescence. This was further validated by depleting gamma interferon (IFN-γ), a cytokine known to control latent toxoplasmosis, in chronically infected prerecrudescent mice. Since CD8(+) T cells (an important source of IFN-γ) lose their functionality during the later phases of chronic toxoplasmosis, we next examined if adoptive transfer of functional CD8(+) T cells from acutely infected donors to the chronically infected prerecrudescent hosts could impede parasite de-encystation and rescue exhausted CD8(+) T cells. While the transfer of immune CD8(+) T cells temporarily restricted the breakdown of cysts, the exhausted endogenous CD8(+) T cell population was not rescued. Over time, the donor population got deleted, resulting in parasite de-encystation and host mortality. Considering that donor CD8(+) T cells fail to become long-lived, one of the cardinal features of memory CD8(+) T cells, it bears the implication that memory CD8 differentiation is impaired during chronic toxoplasmosis. Moreover, our data strongly suggest that while adoptive immunotherapy can prevent parasite de-encystation transiently, reduced antigen burden in the chronic phase by itself is insufficient for rescue of exhausted CD8(+) T cells. The conclusions of this study have profound ramifications in designing immunotherapeutics against chronic toxoplasmosis.
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