Eosinophils Suppress the Migration of T Cells Into the Brain of -Infected Mice and Protect Them From Experimental Cerebral Malaria.

Cerebral malaria is a potentially lethal disease, which is caused by excessive inflammatory responses to parasites. Here we use a newly developed transgenic ANKA () parasite that can be used to study parasite-specific T cell responses. Our present study demonstrates that mice, which lack type I interferon receptor-dependent signaling, are protected from experimental cerebral malaria (ECM) when infected with this novel parasite. Although CD8 T cell responses generated in the spleen are essential for the development of ECM, we measured comparable parasite-specific cytotoxic T cell responses in ECM-protected mice and wild type mice suffering from ECM. Importantly, CD8 T cells were increased in the spleens of ECM-protected mice and the blood-brain-barrier remained intact. This was associated with elevated splenic levels of CCL5, a T cell and eosinophil chemotactic chemokine, which was mainly produced by eosinophils, and an increase in eosinophil numbers. Depletion of eosinophils enhanced CD8 T cell infiltration into the brain and increased ECM induction in -infected mice. However, eosinophil-depletion did not reduce the CD8 T cell population in the spleen or reduce splenic CCL5 concentrations. Our study demonstrates that eosinophils impact CD8 T cell migration and proliferation during -infection in mice and thereby are contributing to the protection from ECM.