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TNF-related apoptosis-inducing ligand (TRAIL)/Apo2L suppresses experimental autoimmune encephalomyelitis in mice.

Authors :
Cretney, Erika
McQualter, Jonathan L.
Kayagaki, Nobuhiko
Yagita, Hideo
Bernard, Claude C. A.
Grewal, Iqbal S.
Ashkenazi, Avi
Smyth, Mark J.
Source :
Immunology & Cell Biology; Oct2005, Vol. 83 Issue 5, p511-519, 9p
Publication Year :
2005

Abstract

Studies have suggested that endogenous TNF-related apoptosis-inducing ligand (TRAIL)/Apo2L may suppress the induction of some autoimmune diseases in mice. Here, we show that TRAIL/Apo2L suppresses autoimmune damage in relapsing-remitting, and non-remitting models of experimental autoimmune encephalomyelitis (EAE). TRAIL/Apo2L-deficient mice and wild-type mice treated with neutralizing anti-TRAIL/Apo2L antibody displayed enhanced clinical score, increased T-cell proliferative responses to myelin oligodendrocyte glycoprotein (MOG), and increased numbers of inflammatory lesions in the spinal cord and central nervous system. TRAIL neutralization immediately before disease onset was most effective at exacerbating disease score. More importantly, therapeutic intervention with recombinant soluble TRAIL/Apo2L delayed the onset and reduced the severity of MOG-induced EAE. These data are the first to illustrate the potential therapeutic value of recombinant TRAIL/Apo2L in suppressing T-cell-mediated autoimmune diseases. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
08189641
Volume :
83
Issue :
5
Database :
Complementary Index
Journal :
Immunology & Cell Biology
Publication Type :
Academic Journal
Accession number :
18096570
Full Text :
https://doi.org/10.1111/j.1440-1711.2005.01358.x