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* Institut National de la Santé et de la Recherche Médicale, Unité 511, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires;
Institut National de la Santé et de la Recherche Médicale, Unité 543, Laboratoire d’Immunologie Cellulaire; and
Laboratoire de Neuropathologie Raymond Escourolle, CHU Pitie-Salpétrière, Université Pierre et Marie Curie, Paris, France
Experimental cerebral malaria (ECM) resulting from Plasmodium berghei ANKA infection involves T lymphocytes. However, the mechanisms of T cell-mediated pathogenesis remain unknown. We found that, in contrast to ECM-susceptible C57BL6 mice, perforin-deficient (PFP-KO) mice were resistant to ECM in the absence of brain lesions, whereas cytoadherence of parasitized erythrocytes and massive accumulation of activated/effector CD8 lymphocytes were observed in both groups of mice. ECM is induced in PFP-KO mice after adoptive transfer of cytotoxic CD8+ cells from infected C57BL6 mice, which were directed to the brain of PFP-KO mice. This specific recruitment might involve chemokine/chemokine receptors, since their expression was up-regulated on activated CD8 cells, and susceptibility to ECM was delayed in CCR5-KO mice. Thus, lymphocyte cytotoxicity and cell trafficking are key players in ECM pathogenesis.
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