ArticleParasite immunology2018
Parasitized Natural Killer cells do not facilitate the spread of Toxoplasma gondii to the brain.
Article in Parasite immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Toxoplasma gondii Dissemination in the Brain Is Facilitated by Infiltrating Peripheral Immune Cells.mBio · 2022Article
- The role of innate lymphoid cells in response to microbes at mucosal surfaces.Mucosal immunology · 2020Review
- Innate Lymphoid Cells in Protection, Pathology, and Adaptive Immunity During Apicomplexan Infection.Frontiers in immunology · 2019Review
- Calling in the CaFrontiers in cellular and infection microbiology · 2019Review
- Parasitized Natural Killer cells do not facilitate the spread of Toxoplasma gondii to the brain.Parasite immunology · 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Toxoplasma gondii is a protozoan parasite capable of invading immune cells and co-opting their migratory pathways to disseminate through the host. Natural Killer (NK) cells can be directly invaded by the parasite and this invasion alters NK cell migration, producing a hypermotile phenotype. However, the consequences of this hypermotile phenotype for the dissemination of T. gondii to the brain remain unknown. To address this, C57BL6/J mice were infected with freshly egressed tachyzoites (type IIPrugniaud strain) or with parasitized NK cells. Under both conditions, parasite loads in the brain were comparable, indicating that parasitized NK cells were not able to facilitate spread of T. gondii to the brain. Consistent with this, we found no evidence for the recruitment of endogenous NK cells to the brain at early time points post-infection, nor any changes in the expression of α4β1 integrin, involved in recruitment of NK cells to the brain. We therefore found no evidence for a role for hypermotile NK cells in delivery of parasites to the brain during acute infection with T. gondii.
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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.