T-lymphocytes response persists following Plasmodium berghei strain Anka infection resolution and may contribute to later experimental cerebral malaria outcomes

J Neuroimmunol. 2019 May 15:330:5-11. doi: 10.1016/j.jneuroim.2019.02.002. Epub 2019 Feb 7.

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.

Keywords: Cerebral malaria; Chloroquine; Glutamate; MK801; Malaria; T lymphocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dizocilpine Maleate / pharmacology
  • Dizocilpine Maleate / therapeutic use
  • Excitatory Amino Acid Antagonists / pharmacology
  • Excitatory Amino Acid Antagonists / therapeutic use
  • Female
  • Malaria, Cerebral / drug therapy*
  • Malaria, Cerebral / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Plasmodium berghei / drug effects*
  • Plasmodium berghei / immunology*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*
  • Treatment Outcome

Substances

  • Excitatory Amino Acid Antagonists
  • Dizocilpine Maleate