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

Erika Cretney, Jonathan Luke McQualter, Nobuhiko Kayagaki, Hideo Yagita, Claude Charles Andre Bernard, Iqbal S Grewal, Avi Ashkenazi, Mark J Smyth

    Research output: Contribution to journalArticleResearchpeer-review

    57 Citations (Scopus)


    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.
    Original languageEnglish
    Pages (from-to)511 - 519
    Number of pages9
    JournalImmunology and Cell Biology
    Issue number5
    Publication statusPublished - 2005

    Cite this