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Identification of novel glycolipid ligands activating a sulfatide-reactive, CD1d-restricted, type II natural killer T lymphocyte

Journal article
Authors Sara Rhost
Linda Löfbom
Britt-Marie Rynmark
B. Pei
Jan-Eric Månsson
Susann Teneberg
Maria K. Blomqvist
Susanna Cardell
Published in European Journal of Immunology
Volume 42
Issue 11
Pages 2851-2860
ISSN 0014-2980
Publication year 2012
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Biomedicine, Department of Microbiology and Immunology
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 2851-2860
Language en
Links dx.doi.org/10.1002/eji.201142350
Keywords Antigens, CD1d, Cell activation, Glycolipid, NKT cells, self-glycolipids, cross-regulation, iinkt cells, recognition, distinct, disease, liver
Subject categories Immunology in the medical area, Microbiology in the medical area

Abstract

Sulfatide-reactive CD1d-restricted natural killer T (NKT) lymphocytes belong to the type II NKT cell subset with diverse TCRs, and have been found to regulate experimental auto-immune encephalomyelitis, tumor immunity, and experimental hepatitis in murine models. NKT cells can be activated by self-lipids presented by CD1d, manifested as autoreactivity. The identity of most of these self-lipids remains unknown. By isolating lipids from a CD1d-expressing, highly stimulatory antigen presenting cell, we identified isoforms of beta-glucosylceramide (GlcCer), with sphingosine and fatty acid chain lengths of C24:0 and C16:0, that activated a sulfatide-reactive type II NKT cell hybridoma. A screen of structurally related glycosphingolipids demonstrated beta-galactosylceramide (GalCer) as another ligand, and further, that the lysoforms were the most potent isoform of the glycosphingo-lipid ligands, followed by isoforms with a long fatty acid chain of C24. Thus, the same type II NKT cell was activated by several ligands, namely sulfatide, GlcCer, and GalCer. However, CD1d-dependent reactivity to antigen presenting cells lacking all GlcCer-based glycosphingolipids, or all glycosphingolipids, was maintained. This suggests that other endogenous, nonglycosphingolipid, lipid ligands contribute to steady-state autoreactivity by type II NKT cells.

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