Critical roles for LIGHT and its Receptors in Generating T cell-mediated immunity during Leishmania donovani infection

Stanley, Amanda C., Rivera, Fabian de Labastida, Haque, Ashraful, Sheel, Meru, Zhou, Yonghong, Amante, Fiona H., Bunn, Patrick T., Randall, Louise M., Pfeffer, Klaus, Scheu, Stefanie, Hickey, Michael J., Saunders, Bernadette M., Ware, Carl, Hill, Geoff R., Tamada, Koji, Kaye, Paul M. and Engwerda, Christian R. (2011) Critical roles for LIGHT and its Receptors in Generating T cell-mediated immunity during Leishmania donovani infection. PLoS Pathogens, 7 10: 1-15. doi:10.1371/journal.ppat.1002279


Author Stanley, Amanda C.
Rivera, Fabian de Labastida
Haque, Ashraful
Sheel, Meru
Zhou, Yonghong
Amante, Fiona H.
Bunn, Patrick T.
Randall, Louise M.
Pfeffer, Klaus
Scheu, Stefanie
Hickey, Michael J.
Saunders, Bernadette M.
Ware, Carl
Hill, Geoff R.
Tamada, Koji
Kaye, Paul M.
Engwerda, Christian R.
Title Critical roles for LIGHT and its Receptors in Generating T cell-mediated immunity during Leishmania donovani infection
Formatted title
Critical roles for LIGHT and its Receptors in Generating T cell-mediated immunity during Leishmania donovani infection
Journal name PLoS Pathogens   Check publisher's open access policy
ISSN 1553-7366
1553-7374
Publication date 2011-10
Sub-type Article (original research)
DOI 10.1371/journal.ppat.1002279
Open Access Status DOI
Volume 7
Issue 10
Start page 1
End page 15
Total pages 15
Place of publication San Francisco, CA, United States
Publisher Public Library of Science
Collection year 2012
Language eng
Formatted abstract
LIGHT (TNFSF14) is a member of the TNF superfamily involved in inflammation and defence against infection. LIGHT signals via two cell-bound receptors; herpes virus entry mediator (HVEM) and lymphotoxin-beta receptor (LTβR). We found that LIGHT is critical for control of hepatic parasite growth in mice with visceral leishmaniasis (VL) caused by infection with the protozoan parasite Leishmania donovani. LIGHT-HVEM signalling is essential for early dendritic cell IL-12/IL-23p40 production, and the generation of IFNγ- and TNF-producing T cells that control hepatic infection. However, we also discovered that LIGHT-LTβR interactions suppress anti-parasitic immunity in the liver in the first 7 days of infection by mechanisms that restrict both CD4+ T cell function and TNF-dependent microbicidal mechanisms. Thus, we have identified distinct roles for LIGHT in infection, and show that manipulation of interactions between LIGHT and its receptors may be used for therapeutic advantage. 
Keyword Tumor Necrosis Factor
Experimental Visceral Leishmaniasis
Herpesvirus Entry Mediator
Lymphotoxin Beta Receptor
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2012 Collection
Institute for Molecular Bioscience - Publications
 
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Citation counts: TR Web of Science Citation Count  Cited 11 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 13 times in Scopus Article | Citations
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