Abstract
Several studies have proposed cerebral malaria (CM) as a CD4+ and CD8+ T lymphocyte-mediated disease. However, there are no data regarding the recruitment and/or persistence of these cells in the CNS following the phase of infection resolution. Glutamate-mediate excitotoxicity has also been implicated in CM. Blockade of glutamate NMDA receptors by its noncompetitive antagonist MK801 modulates cytokine and neurotrophic factors expression preventing cognitive and depressive-like behavior in experimental CM. Herein, we aim to investigate the role of T lymphocytes in later outcomes in CM, and whether the protective role of MK801 is associated with T lymphocytes response.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 5-11 |
| Number of pages | 7 |
| Journal | Journal of Neuroimmunology |
| Volume | 330 |
| DOIs | |
| State | Published - May 15 2019 |
| Externally published | Yes |
Keywords
- Cerebral malaria
- Chloroquine
- Glutamate
- MK801
- Malaria
- T lymphocytes
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology
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