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The Journal of Immunology, 2001, 166: 662-668.
Copyright © 2001 by The American Association of Immunologists

Costimulation-Dependent Modulation of Experimental Autoimmune Encephalomyelitis by Ligand Stimulation of V{alpha}14 NK T Cells1

Endre Pál*, Takeshi Tabira*, Tetsu Kawano{ddagger}, Masaru Taniguchi{ddagger}, Sachiko Miyake{dagger} and Takashi Yamamura2,*,{dagger}

Departments of * Demyelinating Disease and Aging and {dagger} Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan; and {ddagger} CREST Project, Japan Science and Technology Corporation and Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan

Experimental autoimmune encephalomyelitis (EAE) is a Th1 cell-mediated autoimmune disease that can be protected against by stimulating regulatory cells. Here we examined whether EAE can be purposefully modulated by stimulating V{alpha}14 NK T cells with the CD1d-restricted ligand {alpha}-galactosylceramide ({alpha}-GC). EAE induced in wild-type C57BL/6 (B6) mice was not appreciably altered by injection of {alpha}-GC. However, EAE induced in IL-4 knockout mice and IFN-{gamma} knockout mice was enhanced or suppressed by {alpha}-GC, respectively. This indicates that the IL-4 and IFN-{gamma} triggered by {alpha}-GC may play an inhibitory or enhancing role in the regulation of EAE. We next studied whether NK T cells of wild-type mice may switch their Th0-like phenotype toward Th1 or Th2. Notably, in the presence of blocking B7.2 (CD86) mAb, {alpha}-GC stimulation could bias the cytokine profile of NK T cells toward Th2, whereas presentation of {alpha}-GC by CD40-activated APC induced a Th1 shift of NK T cells. Furthermore, transfer of the {alpha}-GC-pulsed APC preparations suppressed or enhanced EAE according to their ability to polarize NK T cells toward Th2 or Th1 in vitro. These results have important implications for understanding the role of NK T cells in autoimmunity and for designing a therapeutic strategy targeting NK T cells.




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