Cutting edge: Selective blockade of LIGHT-lymphotoxin beta receptor signaling protects mice from experimental cerebral malaria caused by Plasmodium berghei ANKA

Randall, Louise M., Amante, Fiona H., Zhou, Yonghong, Stanley, Amanda C., Haque, Ashraful, Rivera, Fabian, Pfeffer, Klaus, Scheu, Stefanie, Hill, Geoff R., Tamada, Koji and Engwerda, Christian R. (2008) Cutting edge: Selective blockade of LIGHT-lymphotoxin beta receptor signaling protects mice from experimental cerebral malaria caused by Plasmodium berghei ANKA. Journal of Immunology, 181 11: 7458-7460. doi:10.4049/jimmunol.181.11.7458


Author Randall, Louise M.
Amante, Fiona H.
Zhou, Yonghong
Stanley, Amanda C.
Haque, Ashraful
Rivera, Fabian
Pfeffer, Klaus
Scheu, Stefanie
Hill, Geoff R.
Tamada, Koji
Engwerda, Christian R.
Title Cutting edge: Selective blockade of LIGHT-lymphotoxin beta receptor signaling protects mice from experimental cerebral malaria caused by Plasmodium berghei ANKA
Journal name Journal of Immunology   Check publisher's open access policy
ISSN 0022-1767
1550-6606
Publication date 2008-12-01
Year available 2008
Sub-type Article (original research)
DOI 10.4049/jimmunol.181.11.7458
Open Access Status Not yet assessed
Volume 181
Issue 11
Start page 7458
End page 7460
Total pages 5
Place of publication Bethesda, MD, U.S.A.
Publisher American Association of Immunologists
Language eng
Subject C1
920109 Infectious Diseases
110803 Medical Parasitology
Abstract Studies in experimental cerebral malaria (ECM) in mice have identified T cells and TNF family members as critical mediators of pathology. In this study we report a role for LIGHT-lymphotoxin beta Receptor (LTbetaR) signaling in the development of ECM and control of parasite growth. Specific blockade of LIGHT-LTbetaR, but not LIGHT-herpesvirus entry mediator interactions, abrogated the accumulation of parasites and the recruitment of pathogenic CD8(+) T cells and monocytes to the brain during infection without affecting early activation of CD4(+) T cells, CD8(+) T cells, or NK cells. Importantly, blockade of LIGHT-LTbetaR signaling caused the expansion of splenic monocytes and an overall enhanced capacity to remove and process Ag during infection, as well as reduced systemic cytokine levels when control mice displayed severe ECM symptoms. In summary, we have discovered a novel pathogenic role for LIGHT and LTbetaR in ECM, identifying this TNF family receptor-ligand interaction as an important immune regulator during experimental malaria.
Keyword Immunology
Immunology
IMMUNOLOGY
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Faculty of Health and Behavioural Sciences -- Publications
2009 Higher Education Research Data Collection
 
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Citation counts: TR Web of Science Citation Count  Cited 16 times in Thomson Reuters Web of Science Article | Citations
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Created: Tue, 24 Mar 2009, 23:32:47 EST by Geraldine Fitzgerald on behalf of School of Public Health