Immune-mediated mechanisms of parasite tissue sequestration during experimental cerebral malaria

Amante, Fiona H., Haque, Ashraful, Stanley, Amanda C., de Labastida Rivera, Fabian, Randall, Louise M., Wilson, Yana A., Yeo, Gladys, Pieper, Christian, Crabb, Brendan S., de Koning-Ward, Tania F., Lundie, Rachel J., Good, Michael F., Pinzon-Charry, Alberto, Pearson, Mark S., Duke, Mary G., McManus, Donald P., Loukas, Alex, Hill, Geoff R. and Engwerda, Christian R. 2010, Immune-mediated mechanisms of parasite tissue sequestration during experimental cerebral malaria, Journal of immunology, vol. 185, no. 6, pp. 3632-3642, doi: 10.4049/jimmunol.1000944.

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Title Immune-mediated mechanisms of parasite tissue sequestration during experimental cerebral malaria
Author(s) Amante, Fiona H.
Haque, Ashraful
Stanley, Amanda C.
de Labastida Rivera, Fabian
Randall, Louise M.
Wilson, Yana A.
Yeo, Gladys
Pieper, Christian
Crabb, Brendan S.
de Koning-Ward, Tania F.ORCID iD for de Koning-Ward, Tania F.
Lundie, Rachel J.
Good, Michael F.
Pinzon-Charry, Alberto
Pearson, Mark S.
Duke, Mary G.
McManus, Donald P.
Loukas, Alex
Hill, Geoff R.
Engwerda, Christian R.
Journal name Journal of immunology
Volume number 185
Issue number 6
Start page 3632
End page 3642
Total pages 11
Publisher American Association of Immunologists
Place of publication Bethesda, Md.
Publication date 2010-09-15
ISSN 0022-1767
Keyword(s) malaria
Summary Cerebral malaria is a severe complication of malaria. Sequestration of parasitized RBCs in brain microvasculature is associated with disease pathogenesis, but our understanding of this process is incomplete. In this study, we examined parasite tissue sequestration in an experimental model of cerebral malaria (ECM). We show that a rapid increase in parasite biomass is strongly associated with the induction of ECM, mediated by IFN-γ and lymphotoxin α, whereas TNF and IL-10 limit this process. Crucially, we discovered that host CD4+ and CD8+ T cells promote parasite accumulation in vital organs, including the brain. Modulation of CD4+ T cell responses by helminth coinfection amplified CD4+ T cell-mediated parasite sequestration, whereas vaccination could generate CD4+ T cells that reduced parasite biomass and prevented ECM. These findings provide novel insights into immune-mediated mechanisms of ECM pathogenesis and highlight the potential of T cells to both prevent and promote infectious diseases.
Notes Published online before print August 18, 2010
Language eng
DOI 10.4049/jimmunol.1000944
Field of Research 110707 Innate Immunity
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2010, American Association of Immunologists
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Document type: Journal Article
Collection: School of Medicine
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