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

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. [Display omitted] •T-lymphocytes remain in the brain of CM mice following PbA infection resolution.•MK801 restore the percentage of TCD4+ expressing IL-10 in the brain of Pba-infected mice.•MK801 decreases the percentage of TCD4+ expressing TNF in the brain of Pba-infected mice.•MK801 decreases the percentage of TCD8+ expressing IFN-γ and TNF in the brain of Pba-infected mice.