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Updated: Sep 28, 2026
Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
On the pathogenic role of brain-sequestered alphabeta CD8+ T cells in experimental cerebral malaria
Elodie Belnoue1, Michèle Kayibanda, Ana M Vigario
1Département d'Immunologie, Institut Cochin, Institut National de la Santé et de la Recherche Médicale Unité 567, Centre National de la Recherche Scientifique Unité Mixte de Recherche 8104, Hôpital Cochin, Université René Descartes, Paris, France.
Abstract:
Cerebral malaria (CM) develops in a small proportion of persons infected with Plasmodium falciparum and accounts for a substantial proportion of the mortality due to this parasite. The actual pathogenic mechanisms are still poorly understood, and in humans investigations of experimental CM are unethical. Using an established Plasmodium berghei-mouse CM model, we have investigated the role of host immune cells at the pathological site, the brain. We report in this study the detailed quantification and characterization of cells, which migrated and sequestered to the brain of mice with CM. We demonstrated that CD8(+) alphabeta T cells, which sequester in the brain at the time when neurological symptoms appear, were responsible for CM mortality. These observations suggest a mechanism which unifies disparate observations in humans.
Insights
Cerebral malaria (CM) mortality is caused by CD8(+) alphabeta T cells sequestering in the brain. This study identifies key immune cells responsible for severe malaria pathology in a mouse model.
Area of Science:
- Immunology
- Neuroscience
- Infectious Diseases
Background:
- Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, causing significant mortality.
- The precise pathogenic mechanisms underlying CM remain poorly understood.
- Ethical constraints limit direct investigation of experimental CM in humans.
Purpose of the Study:
- To investigate the role of host immune cells in the pathogenesis of CM.
- To characterize the cells that infiltrate and sequester within the brain during CM.
- To elucidate the cellular mechanisms contributing to CM-associated mortality.
Main Methods:
- Utilized a Plasmodium berghei mouse model of experimental CM.
- Performed detailed quantification and characterization of immune cells in the brain.
- Focused on immune cell populations present during the onset of neurological symptoms.
Main Results:
- Identified and quantified specific immune cell populations within the brain during CM.
- Demonstrated the sequestration of CD8(+) alphabeta T cells in the brain.
- Correlated the presence of these T cells with the appearance of neurological symptoms and mortality.
Conclusions:
- CD8(+) alphabeta T cells are critically involved in causing mortality in experimental CM.
- Brain-sequestered CD8(+) alphabeta T cells are a key factor in CM pathogenesis.
- These findings offer a unifying mechanism for disparate observations in human CM.
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