| Literature DB >> 29625893 |
Kristina S Burrack1, Matthew A Huggins2, Emily Taras3, Philip Dougherty3, Christine M Henzler4, Rendong Yang4, Sarah Alter5, Emily K Jeng5, Hing C Wong5, Martin Felices3, Frank Cichocki3, Jeffrey S Miller3, Geoffrey T Hart6, Aaron J Johnson7, Stephen C Jameson1, Sara E Hamilton8.
Abstract
Cerebral malaria is a deadly complication of Plasmodium infection and involves blood brain barrier (BBB) disruption following infiltration of white blood cells. During experimental cerebral malaria (ECM), mice inoculated with Plasmodium berghei ANKA-infected red blood cells develop a fatal CM-like disease caused by CD8+ T cell-mediated pathology. We found that treatment with interleukin-15 complex (IL-15C) prevented ECM, whereas IL-2C treatment had no effect. IL-15C-expanded natural killer (NK) cells were necessary and sufficient for protection against ECM. IL-15C treatment also decreased CD8+ T cell activation in the brain and prevented BBB breakdown without influencing parasite load. IL-15C induced NK cells to express IL-10, which was required for IL-15C-mediated protection against ECM. Finally, we show that ALT-803, a modified human IL-15C, mediates similar induction of IL-10 in NK cells and protection against ECM. These data identify a regulatory role for cytokine-stimulated NK cells in the prevention of a pathogenic immune response.Entities:
Keywords: CD8(+) T cells; IL-10; IL-15; NK cells; cerebral malaria; cytokine complexes; immunopathology
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Year: 2018 PMID: 29625893 PMCID: PMC5906161 DOI: 10.1016/j.immuni.2018.03.012
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 43.474