title: [The role of sulfatides in autoimmunity in children with various glomerular disease].
abstract: Previous studies have suggested that autoimmunity to a number of kidney antigens may exist in glomerular disease. Our own work suggested that sulfatide which is one of the major acidic glycolipids of human kidney may be antigenic. Glycolipids were isolated from lipid extract of human kidney using thin-layer chromatography (TLC). As the major acidic glycolipids, sulfatide, CDH-sulfate, GM3, GD3 were identified. Acidic fraction of lipid extract were chromatographed and then tested for antigen by immunostaining. Sera from patients with IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis (HSPN) contained antibody to the sulfatide of human kidney as determined by the direct binding of antibody to TLC. In addition, we measured the presence of sulfatide antibodies by enzyme linked immunosorbent assay (ELISA) in sera of patients with various glomerular disease: IgAN, HSPN, mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis (MPGN), focal and segmental glomeruosclerosis (FSGS), membranous nephropathy (MN), minimal change nephrotic syndrome (MCNS), acute post streptococcal glomerulonephritis (PSAGN), and lupus nephritis (LN). IgM class sulfatide antibody were demonstrated in many cases of them. The incidence of IgA class sulfatide antibody in HSPN and IgAN was significantly high, and also the high incidence of IgG class sulfatide antibody occurred in IgAN. On the other hand, we evaluated cellular hypersensitivity to sulfatide in IgAN, HSPN, and FSGS using an active E-rosette assay. Positive results occurred in IgAN and HSPN. It was suggested that delayed hypersensitivity to sulfatide may generate an autoimmune inflammatory process. It has been reported that laminin binds specifically to sulfatide. Autoimmunity to sulfatide may disturb the laminin binding and consequently interfere with renal function. These results suggested sulfatide antigen may play important role in occurrence and aggravation of glomerular disease.
authors.affiliation: Department of Pediatrics, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Tamaoki
authors.forename: Y
authors.initials: Y
authors.lastname: Kikkawa
mesh_terms: D000293:Adolescent; D015551:Autoimmunity; D002648:Child; D002675:Child, Preschool; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005921:Glomerulonephritis / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D007136:Immunoglobulins / Q000032:analysis; D008297:Male; D012397:Rosette Formation; D013433:Sulfoglycosphingolipids / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D007136:Immunoglobulins; D013433:Sulfoglycosphingolipids