Costimulation-Dependent Modulation of Experimental Autoimmune Encephalomyelitis by Ligand Stimulation of Vα14 NK T Cells

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  • Endre Pál
    Demyelinating Disease and Aging, National Center of Neurology and Psychiatry , Kodaira, Tokyo ,
  • Takeshi Tabira
    Demyelinating Disease and Aging, National Center of Neurology and Psychiatry , Kodaira, Tokyo ,
  • Tetsu Kawano
    CREST Project, Japan Science and Technology Corporation and Department of Molecular Immunology, Graduate School of Medicine, Chiba University , Chuo-ku, Chiba ,
  • Masaru Taniguchi
    CREST Project, Japan Science and Technology Corporation and Department of Molecular Immunology, Graduate School of Medicine, Chiba University , Chuo-ku, Chiba ,
  • Sachiko Miyake
    Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry , Kodaira, Tokyo ,
  • Takashi Yamamura
    Demyelinating Disease and Aging, National Center of Neurology and Psychiatry , Kodaira, Tokyo ,

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公開日
2001-01-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.166.1.662
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>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 Vα14 NK T cells with the CD1d-restricted ligand α-galactosylceramide (α-GC). EAE induced in wild-type C57BL/6 (B6) mice was not appreciably altered by injection of α-GC. However, EAE induced in IL-4 knockout mice and IFN-γ knockout mice was enhanced or suppressed by α-GC, respectively. This indicates that the IL-4 and IFN-γ triggered by α-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, α-GC stimulation could bias the cytokine profile of NK T cells toward Th2, whereas presentation of α-GC by CD40-activated APC induced a Th1 shift of NK T cells. Furthermore, transfer of the α-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.</jats:p>

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