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A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells

Author

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  • Katsuichi Miyamoto

    (National Institute of Neuroscience, NCNP)

  • Sachiko Miyake

    (National Institute of Neuroscience, NCNP)

  • Takashi Yamamura

    (National Institute of Neuroscience, NCNP)

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a prototype autoimmune disease mediated by type 1 helper T (TH1) cells and under the control of regulatory cells1,2,3. Here we report that a synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14+) is preventive against EAE. The ligand is an analogue of α-galactosylceramide (α-GC), a prototype NKT cell ligand, with a truncated sphingosine chain. α-GC causes NKT cells to produce both interferon (IFN)-γ and interleukin (IL)-4 (refs 4, 5). However, this new ligand can induce a predominant production of IL-4 by the NKT cells. A single injection of this glycolipid, but not of α-GC, consistently induced TH2 bias of autoimmune T cells by causing NKT cells to produce IL-4, leading to suppression of EAE. The lack of polymorphism of CD1d and cross-reactive response of mouse and human NKT cells to the same ligand6 indicates that targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.

Suggested Citation

  • Katsuichi Miyamoto & Sachiko Miyake & Takashi Yamamura, 2001. "A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells," Nature, Nature, vol. 413(6855), pages 531-534, October.
    • Handle: RePEc:nat:nature:v:413:y:2001:i:6855:d:10.1038_35097097
    DOI: 10.1038/35097097
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    Cited by:

    1. Ann-Christin Gnirck & Marie-Sophie Philipp & Alex Waterhölter & Malte Wunderlich & Nikhat Shaikh & Virginia Adamiak & Lena Henneken & Tobias Kautz & Tingting Xiong & Daniela Klaus & Pascal Tomczyk & M, 2023. "Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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