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Administration of Sulfatide to Ameliorate Type I Diabetes in Non‐Obese Diabetic Mice
Author(s) -
Rhost S.,
Löfbom L.,
Månsson J.E.,
Lehuen A.,
Blomqvist M.,
Cardell S. L.
Publication year - 2014
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12157
Subject(s) - autoantibody , nod mice , immune system , medicine , nod , endocrinology , type 1 diabetes , immunology , diabetes mellitus , autoimmunity , antibody
The endogenous glycosphingolipid sulfatide is a ligand for CD 1d‐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 co‐localizes with insulin within the Langerhans islet β ‐cells, targets for the immune destruction in type 1 diabetes ( T 1 D ). Human T 1 D 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 T 1 D in humans. Here, we investigate sulfatide as an autoantigen and a modulator of autoimmune disease in the murine model for T 1 D , 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 T 1 D . 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 T 1 D 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 T 1 D in this mouse strain.