ArticleThe American journal of pathology2011
Protein kinase C-theta is required for development of experimental cerebral malaria.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Inhibition ofBiomedicines · 2025Article
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Cerebral Malaria: Current Clinical and Immunological Aspects.Frontiers in immunology · 2022Review
- MRI demonstrates glutamine antagonist-mediated reversal of cerebral malaria pathology in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria.PLoS pathogens · 2017Article
- Host-pathogen interactions in malaria: cross-kingdom signaling and mitochondrial regulation.Current opinion in immunology · 2015Review
- IL-33-mediated protection against experimental cerebral malaria is linked to induction of type 2 innate lymphoid cells, M2 macrophages and regulatory T cells.PLoS pathogens · 2015Article
- Phosphatidylinositol 3-Kinase γ is required for the development of experimental cerebral malaria.PloS one · 2015Article
- Stable tumor vessel normalization with pO₂ increase and endothelial PTEN activation by inositol trispyrophosphate brings novel tumor treatment.Journal of molecular medicine (Berlin, Germany) · 2013Article
- DOR activation inhibits anoxic/ischemic Na+ influx through Na+ channels via PKC mechanisms in the cortex.Experimental neurology · 2012Article
- Involvement of distinct PKC gene products in T cell functions.Frontiers in immunology · 2012Article
- In the eye of experimental cerebral malaria.The American journal of pathology · 2011Article
- The protective effects of curcumin in cerebral ischemia and reperfusion injury through PKC-θ signaling.Cell cycle (Georgetown, Tex.)Article
- Steroid Pulse Therapy May Mitigate Prolonged Neurological Manifestations after Eradication of Severe Plasmodium falciparum Parasitemia.Internal medicine (Tokyo, Japan)Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral malaria is the most severe neurologic complication in children and young adults infected with Plasmodium falciparum. T-cell activation is required for development of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (CM). To characterize the T-cell activation pathway involved, the role of protein kinase C-theta (PKC-θ) in experimental CM development was examined. PKC-θ-deficient mice are resistant to CM development. In the absence of PKC-θ, no neurologic sign of CM developed after blood stage PbA infection. Resistance of PKC-θ-deficient mice correlated with unaltered cerebral microcirculation and absence of ischemia, as documented by magnetic resonance imaging and magnetic resonance angiography, whereas wild-type mice developed distinct microvascular pathology. Recruitment and activation of CD8(+) T cells, and ICAM-1 and CD69 expression were reduced in the brain of resistant mice; however, the pulmonary inflammation and edema associated with PbA infection were still present in the absence of functional PKC-θ. Resistant PKC-θ-deficient mice developed high parasitemia, and died at 3 weeks with severe anemia. Therefore, PKC-θ signaling is crucial for recruitment of CD8(+) T cells and development of brain microvascular pathology resulting in fatal experimental CM, and may represent a novel therapeutic target of CM.
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