Cell-specific MHC class I deletion on CD11c+ APCs abrogates CD8 T Cell infiltration into the brain

Abstract Cerebral malaria (CM) is a severe complication of P. falciparum infection and leading cause death, globally. Plasmodium berghei ANKA (PbA) C57BL/6 mice serves as murine model CM called experimental cerebral (ECM) due to the neurological neuropathological features that simulate human CM. A putative mechanism disease in requires CD8 T cell infiltration into brain blood-brain barrier disruption. The specific antigen-presenting type(s) prime this CNS infiltrating response capable inducing lethal disruption has not been defined. To answer this, single class I expressing K bloxP transgenic were generated. Crossing these deficient CD11c-cre or LysM-cre created bcKO mice, respectively. PbA infected susceptible ECM. In contrast, survived acute avoided manifestations. We therefore employed spectral flow cytometry analyze splenocytes immune cells during genotypes. observed reduction activated spleens versus bcKO. This reduced peripheral activation Kb cKO also corresponded with cells. conclude CD11c+ APC required for priming potentially recruitment ECM pathology. 5R01NS103212-06