caa a22 4500 469128852 CHVBK 20180323133158.0 cr unu---uuuuu 170328e19920601xx s 000 0 eng 10.1007/BF00572546 doi (NATIONALLICENCE)springer-10.1007/BF00572546 Which glycolipids are the autoantigens of cytoplasmatic islet cell antibodies? [Elektronische Daten] [E. Cabrera, L. Fernandez, A. Carr, G. Marquina, O. Valiente, A. Uriarte, B. Rynmark, P. Fredman, L. Svennerholm] It has been suggested that acidic glycolipids may be the target of autoimmune phenomena in type 1 diabetes. The aim of the present study was to provide a better understanding of the nature and the chemical structure of pancreatic glycolipids reacting with antibodies from type 1 diabetic patients. Gangliosides and other acidic glycolipids were extracted from human pancreas in chloroform-methanol-water and separated on fractogel TSK DEAE columns. Separated glycolipids were tested for their ability to block islet cell antibody (ICA) binding on frozen pancreatic sections. Furthermore, pancreatic acidic glycolipids and standard gangliosides and sulphatides were used as the substrate for immunostaining on thin layer chromatography (TLC) plates, using ICA-positive and ICA-negative sera. ICA binding was blocked by pancreatic acidic glycolipids even though the alkali treated lipid extract pointed to the alkali-stable acidic glycolipid character of the molecules involved in the blocking effect. ICA+ sera specifically reacted on TLC plates with two pancreatic acidic glycolipids, one migrating with the solvent front and the other with a mobility between GM2 and GM1 standards. None of the ICA-positive sera reacted with standard gangliosides (3′-LM1, 3′-isoLM1, GM1, GD1a, GD1b, GT1b). In addition, ICA+ sera reacted with different standard sulphated glycolipids. In conclusion, our results suggest that not only gangliosides, but also sulphatides, are targets of type 1 diabetes-associated antibodies. Springer-Verlag, 1992 Islet cell antibodies nationallicence Gangliosides nationallicence Sulphated glycolipids nationallicence Autoantigen nationallicence Cabrera E. National Institute of Endocrinology, Havana, Cuba aut Fernandez L. Centre for Molecular Immunology, Havana, Cuba aut Carr A. Centre for Molecular Immunology, Havana, Cuba aut Marquina G. Centre for Molecular Immunology, Havana, Cuba aut Valiente O. Centre for Molecular Immunology, Havana, Cuba aut Uriarte A. National Institute of Endocrinology, Havana, Cuba aut Rynmark B. University of Gothenburg, Gothenburg, Sweden aut Fredman P. University of Gothenburg, Gothenburg, Sweden aut Svennerholm L. University of Gothenburg, Gothenburg, Sweden aut Acta Diabetologica Springer-Verlag 29/2(1992-06-01), 70-74 0940-5429 29:2<70 1992 29 592 https://doi.org/10.1007/BF00572546 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00572546 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Cabrera E. National Institute of Endocrinology, Havana, Cuba aut NATIONALLICENCE 700 1- Fernandez L. Centre for Molecular Immunology, Havana, Cuba aut NATIONALLICENCE 700 1- Carr A. Centre for Molecular Immunology, Havana, Cuba aut NATIONALLICENCE 700 1- Marquina G. Centre for Molecular Immunology, Havana, Cuba aut NATIONALLICENCE 700 1- Valiente O. Centre for Molecular Immunology, Havana, Cuba aut NATIONALLICENCE 700 1- Uriarte A. National Institute of Endocrinology, Havana, Cuba aut NATIONALLICENCE 700 1- Rynmark B. University of Gothenburg, Gothenburg, Sweden aut NATIONALLICENCE 700 1- Fredman P. University of Gothenburg, Gothenburg, Sweden aut NATIONALLICENCE 700 1- Svennerholm L. University of Gothenburg, Gothenburg, Sweden aut NATIONALLICENCE 773 0- Acta Diabetologica Springer-Verlag 29/2(1992-06-01), 70-74 0940-5429 29:2<70 1992 29 592 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer