ArticlePloS one2008
Both functional LTbeta receptor and TNF receptor 2 are required for the development of experimental cerebral malaria.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Experimental Models to Study the Pathogenesis of Malaria-Associated Acute Respiratory Distress Syndrome.Frontiers in cellular and infection microbiology · 2022Review
- Using two phases of the CD4 T cell response to blood-stage murine malaria to understand regulation of systemic immunity and placental pathology in Plasmodium falciparum infection.Immunological reviews · 2020Review
- EphA2 contributes to disruption of the blood-brain barrier in cerebral malaria.PLoS pathogens · 2020Article
- Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- The Glycosylphosphatidylinositol Transamidase Complex Subunit PbGPI16 of Plasmodium berghei Is Important for Inducing Experimental Cerebral Malaria.Infection and immunity · 2018Article
- The LymphotoxinMediators of inflammation · 2017Article
- Myeloid expression of the AP-1 transcription factor JUNB modulates outcomes of type 1 and type 2 parasitic infections.Parasite immunology · 2015Article
- Role of the Lymphotoxin/LIGHT System in the Development and Maintenance of Reticular Networks and Vasculature in Lymphoid Tissues.Frontiers in immunology · 2014Review
- Lipoxin A₄ and 15-epi-lipoxin A₄ protect against experimental cerebral malaria by inhibiting IL-12/IFN-γ in the brain.PloS one · 2013Article
- In the eye of experimental cerebral malaria.The American journal of pathology · 2011Article
- Article
- Peroxisome proliferator activating receptor (PPAR) in cerebral malaria (CM): a novel target for an additional therapy.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2011Review
- Host resistance to malaria: using mouse models to explore the host response.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Review
- Protein kinase C-theta is required for development of experimental cerebral malaria.The American journal of pathology · 2011Article
- Glioma morphology and tumor-induced vascular alterations revealed in seven rodent glioma models by in vivo magnetic resonance imaging and angiography.Journal of magnetic resonance imaging : JMRI · 2010Article
- 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
17 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTNF-related lymphotoxin alpha (LTalpha) is essential for the development of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM). The pathway involved has been attributed to TNFR2. Here we show a second arm of LTalpha-signaling essential for ECM development through LTbeta-R, receptor of LTalpha1beta2 heterotrimer. METHODOLOGY/PRINCIPAL
findingsLTbetaR deficient mice did not develop the neurological signs seen in PbA induced ECM but died at three weeks with high parasitaemia and severe anemia like LTalphabeta deficient mice. Resistance of LTalphabeta or LTbetaR deficient mice correlated with unaltered cerebral microcirculation and absence of ischemia, as documented by magnetic resonance imaging and angiography, associated with lack of microvascular obstruction, while wild-type mice developed distinct microvascular pathology. Recruitment and activation of perforin(+) CD8(+) T cells, and their ICAM-1 expression were clearly attenuated in the brain of resistant mice. An essential contribution of LIGHT, another LTbetaR ligand, could be excluded, as LIGHT deficient mice rapidly succumbed to ECM. CONCLUSIONS/SIGNIFICANCE: LTbetaR expressed on radioresistant resident stromal, probably endothelial cells, rather than hematopoietic cells, are essential for the development of ECM, as assessed by hematopoietic reconstitution experiment. Therefore, the data suggest that both functional LTbetaR and TNFR2 signaling are required and non-redundant for the development of microvascular pathology resulting in fatal ECM.
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