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*
Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, and
Core Research for Evolutional Science and Technology Program of the Japan Science and Technology Corporation, Sendai, Japan
OX40 ligand (OX40L) expressed on APCs, and its receptor, OX40
present on activated T cells, are members of the TNF/TNFR family,
respectively, and have been located at the sites of inflammatory
conditions. We have observed in OX40L-deficient mice
(OX40L-/-) an impaired APC capacity and in our recently
constructed transgenic mice expressing OX40L (OX40L-Tg), a markedly
enhanced T cell response to protein Ags. Using these mice, we
demonstrate here the critical involvement of the OX40L-OX40 interaction
during the T cell priming events in the occurrence of experimental
autoimmune encephalomyelitis (EAE). In OX40L-/- mice,
abortive T cell priming greatly reduced the clinical manifestations of
actively induced EAE, coupled with a reduction in IFN-
, IL-2, and
IL-6 production in vitro. Adoptive transfer experiments however
revealed an efficient transfer of disease to OX40L-/-
mice using wild-type donor T cells, indicating an intact capacity of
OX40L-/- mice to initiate effector responses. On the
other hand, OX40L-/- donor T cells failed to transfer
disease to wild-type recipient mice. Furthermore, OX40L-Tg mice
developed a greater severity of EAE despite a delayed onset, while both
OX40L-Tg/CD28-/- and OX40L-Tg/CD40-/- mice
failed to develop EAE demonstrating a requisite for these molecules.
These findings indicate a pivotal role played by OX40L in the
pathogenesis of EAE.
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