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Multiple tissue-specific isoforms of sulfatide activate CD1d-restricted type II NKT cells.

Journal article
Authors Maria K. Blomqvist
Sara Rhost
Susann Teneberg
Linda Löfbom
Thomas Osterbye
Manfred Brigl
Jan-Eric Månsson
Susanna Cardell
Published in European journal of immunology
Volume 39
Issue 7
Pages 1726-35
ISSN 1521-4141
Publication year 2009
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 1726-35
Language en
Keywords Animals, Antigen-Presenting Cells, cytology, immunology, Antigens, CD1d, genetics, immunology, Cells, Cultured, Dendritic Cells, cytology, immunology, Enzyme-Linked Immunosorbent Assay, Fatty Acids, chemistry, immunology, Flow Cytometry, Hybridomas, immunology, Mice, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Knockout, Natural Killer T-Cells, cytology, immunology, metabolism, Spleen, cytology, immunology, metabolism, Sulfoglycosphingolipids, chemistry, immunology, metabolism
Subject categories Microbiology in the medical area, Chemistry


The glycosphingolipid sulfatide (SO(3)-3Galbeta1Cer) is a demonstrated ligand for a subset of CD1d-restricted NKT cells, which could regulate experimental autoimmune encephalomyelitis, a murine model for multiple sclerosis, as well as tumor immunity and experimental hepatitis. Native sulfatide is a mixture of sulfatide isoforms, i.e. sulfatide molecules with different long-chain bases and fatty acid chain lengths and saturation. Here, we demonstrate that sulfatide-specific CD1d-restricted murine NKT hybridomas recognized several different sulfatide isoforms. These included the physiologically relevant isoforms C24:1 and C24:0, major constituents of the myelin sheet of the nervous system, and C16:0, prominent in the pancreatic islet beta-cells. The most potent sulfatide isoform was lysosulfatide (lacking a fatty acid). Shortened fatty acid chain length (C24:1 versus C18:1), or saturation of the long fatty acid (C24:0), resulted in reduced stimulatory capacity, and fatty acid hydroxylation abolished the response. Moreover, sulfatide was not responsible for the natural autoreactivity toward splenocytes by XV19 T hybridoma cells. Our results reveal a promiscuity in the recognition of sulfatide isoforms by a CD1d-restricted NKT-cell clone, and suggest that sulfatide, a major component of the myelin sheet and pancreatic beta-cells, is one of several natural ligands for type II CD1d-restricted NKT cells.

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