Lysosomal Glycosphingolipid Recognition by NKT Cells

DOI Web Site 被引用文献37件
  • Dapeng Zhou
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Jochen Mattner
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Carlos Cantu
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Nicolas Schrantz
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Ning Yin
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Ying Gao
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Yuval Sagiv
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Kelly Hudspeth
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Yun-Ping Wu
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Tadashi Yamashita
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Susann Teneberg
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Dacheng Wang
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Richard L. Proia
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Steven B Levery
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Paul B. Savage
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Luc Teyton
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.
  • Albert Bendelac
    University of Chicago, Department of Pathology, Chicago, IL 60637, USA.

抄録

<jats:p>NKT cells represent a distinct lineage of T cells that coexpress a conserved αβ T cell receptor (TCR) and natural killer (NK) receptors. Although the TCR of NKT cells is characteristically autoreactive to CD1d, a lipid-presenting molecule, endogenous ligands for these cells have not been identified. We show that a lysosomal glycosphingolipid of previously unknown function, isoglobotrihexosylceramide (iGb3), is recognized both by mouse and human NKT cells. Impaired generation of lysosomal iGb3 in mice lacking β-hexosaminidase b results in severe NKT cell deficiency, suggesting that this lipid also mediates development of NKT cells in the mouse. We suggest that expression of iGb3 in peripheral tissues may be involved in controlling NKT cell responses to infections and malignancy and in autoimmunity.</jats:p>

収録刊行物

  • Science

    Science 306 (5702), 1786-1789, 2004-12-03

    American Association for the Advancement of Science (AAAS)

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