Lysosomal Glycosphingolipid Recognition by NKT Cells-Reference-Cited by-同舟云学术

Lysosomal Glycosphingolipid Recognition by NKT Cells

Published:2004-12-03 Issue:5702 Volume:306 Page:1786-1789
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Zhou Dapeng¹²³⁴⁵,Mattner Jochen¹²³⁴⁵,Cantu Carlos¹²³⁴⁵,Schrantz Nicolas¹²³⁴⁵,Yin Ning¹²³⁴⁵,Gao Ying¹²³⁴⁵,Sagiv Yuval¹²³⁴⁵,Hudspeth Kelly¹²³⁴⁵,Wu Yun-Ping¹²³⁴⁵,Yamashita Tadashi¹²³⁴⁵,Teneberg Susann¹²³⁴⁵,Wang Dacheng¹²³⁴⁵,Proia Richard L.¹²³⁴⁵,Levery Steven B¹²³⁴⁵,Savage Paul B.¹²³⁴⁵,Teyton Luc¹²³⁴⁵,Bendelac Albert¹²³⁴⁵

Affiliation:

1. University of Chicago, Department of Pathology, Chicago, IL 60637, USA.

2. The Scripps Research Institute, Department of Immunology, La Jolla, CA 92037, USA.

3. Brigham Young University, Department of Chemistry and Biochemistry, Provo, UT 84602–5700, USA.

4. Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.

5. Institute of Medical Biochemistry, Göteborg University, SE 405 30 Göteborg, Sweden.

Abstract

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference34 articles.

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