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Administration of sulfatide to ameliorate type I diabetes in non-obese diabetic mice.

Journal article
Authors Sara Rhost
Linda Löfbom
Jan-Eric Månsson
A Lehuen
Maria K. Blomqvist
Susanna Cardell
Published in Scandinavian journal of immunology
Volume 79
Issue 4
Pages 260-6
ISSN 1365-3083
Publication year 2014
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Biomedicine, Department of Microbiology and Immunology
Pages 260-6
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Animals, Antigens, CD1d, metabolism, Autoantibodies, blood, Cytotoxicity, Immunologic, Diabetes Mellitus, Type 1, drug therapy, immunology, Disease Models, Animal, Disease Progression, Female, Galactosylceramides, administration & dosage, Humans, Islets of Langerhans, metabolism, Mice, Mice, Inbred NOD, Natural Killer T-Cells, immunology, Sulfoglycosphingolipids, administration & dosage
Subject categories Immunology in the medical area

Abstract

The endogenous glycosphingolipid sulfatide is a ligand for CD1d-restricted type II natural killer T (NKT) lymphocytes. Through the action of these cells,sulfatide treatment has been shown to modulate the immune response in mouse models for autoimmune diseases, infections and tumour immunity. Sulfatide exists naturally in different organs including the pancreas, where sulfatide colocalizes with insulin within the Langerhans islet b-cells, targets for the immune destruction in type 1 diabetes (T1D). Human T1D patients, but not patients with type 2 diabetes nor healthy individuals, have autoantibodies against sulfatide in serum, suggesting that sulfatide induces an immune response in the natural course of T1D in humans. Here, we investigate sulfatide as an autoantigen and a modulator of autoimmune disease in the murine model forT1D, the non-obese diabetic (NOD) mice. We demonstrate that aged NOD mice displayed serum autoantibody reactivity to sulfatide; however, this reactivity did not correlate with onset of T1D. Repeated administration of sulfatide did not result in an increase in serum reactivity to sulfatide. Moreover, a multidose sulfatide treatment of female NOD mice initiated at an early (5 weeks of age),intermediate (8 weeks of age) or late (12 weeks of age) phase of T1D progression did not influence the incidence of disease. Thus, we demonstrate that a fraction of NOD mice develop autoantibody reactivity to sulfatide; however, we fail to demonstrate that sulfatide treatment reduces the incidence of T1D in this mouse strain.

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