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TNF‐related apoptosis‐inducing ligand (TRAIL)/Apo2L suppresses experimental autoimmune encephalomyelitis in mice
Author(s) -
Cretney Erika,
McQualter Jonathan L,
Kayagaki Nobuhiko,
Yagita Hideo,
Bernard Claude CA,
Grewal Iqbal S,
Ashkenazi Avi,
Smyth Mark J
Publication year - 2005
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/j.1440-1711.2005.01358.x
Subject(s) - myelin oligodendrocyte glycoprotein , experimental autoimmune encephalomyelitis , multiple sclerosis , immunology , medicine , autoimmune disease , tumor necrosis factor alpha , recombinant dna , encephalomyelitis , fas ligand , myelin , apoptosis , central nervous system , antibody , biology , endocrinology , programmed cell death , biochemistry , gene
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.