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,
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Departments of Neurology and
Immunology, Juntendo University School of Medicine, Tokyo, Japan;
Core Research for Evolutional Science and Technology of Japan Science and Technology Corp., Tokyo, Japan;
Department of Joint Disease and Rheumatism, Nippon Medical School, Tokyo, Japan;
¶ Third Department of Medicine (Neurology), Shinshu University School of Medicine, Matsumoto, Japan; and
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Department of Surgery, Faculty of Medicine, University of Tokyo, Tokyo, Japan
OX40 (CD134) and its ligand (OX40L) have been implicated in T cell
activation and migration. In this study, we examined the contribution
of these molecules to the pathogenesis of experimental autoimmune
encephalomyelitis (EAE) by administering a neutralizing mAb against
murine OX40L (RM134L) to proteolipid protein (139–151) peptide-induced
EAE in SJL mice. Administration of RM134L effectively ameliorated the
disease in both actively induced and adoptively transferred EAE models.
Histological examination showed that the RM134L treatment greatly
reduced mononuclear cell infiltration into the spinal cord. The RM134L
treatment did not inhibit the development of pathogenic T cells, given
that proliferative response and IFN-
production by draining lymph
node cells were not reduced or rather enhanced upon restimulation with
proteolipid protein (139–151) in vitro, and these cells effectively
transferred EAE to naive SJL mice. Flow cytometric analyses showed that
the RM134L treatment inhibited the accumulation of OX40-expressing
CD4+ T cells and the migration of adoptively transferred
CD4+ T cells in the spinal cord. Immunohistochemical
staining showed that OX40L was most prominently expressed on
endothelial cells in the inflamed spinal cord. These results suggest
that the OX40/OX40L interaction plays a critical role for the migration
of pathogenic T cells into the CNS in the pathogenesis of
EAE.
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