Gluten exacerbates IgA nephropathy in humanized mice through gliadin–CD89 interaction

• Published in: Kidney international Vol. 88; no. 2; pp. 276 - 285
• Main Authors: Papista, Christina, Lechner, Sebastian, Ben Mkaddem, Sanae, LeStang, Marie-Bénédicte, Abbad, Lilia, Bex-Coudrat, Julie, Pillebout, Evangéline, Chemouny, Jonathan M., Jablonski, Mathieu, Flamant, Martin, Daugas, Eric, Vrtovsnik, François, Yiangou, Minas, Berthelot, Laureline, Monteiro, Renato C.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.08.2015; Elsevier Limited
• Subjects: Animals; Antigens, CD - blood; Antigens, CD - metabolism; Atrophy - etiology; Diet, Gluten-Free; Disease Models, Animal; Enteritis - etiology; Gliadin - immunology; Gliadin - metabolism; glomerulonephritis; Glomerulonephritis, IGA - diet therapy; Glomerulonephritis, IGA - immunology; Glomerulonephritis, IGA - metabolism; Glutens - administration & dosage; Glutens - immunology; Glutens - toxicity; GTP-Binding Proteins - metabolism; Hematuria - diet therapy; Hematuria - etiology; IgA nephropathy; Immunoglobulin A - blood; Immunoglobulin A - metabolism; inflammation; Intestinal Mucosa - immunology; Intestinal Mucosa - pathology; Intestinal Mucosa - secretion; Male; Mice; mucosal immunity; Proteinuria - etiology; Receptors, Fc - blood; Receptors, Fc - metabolism; Receptors, Transferrin - metabolism; Transglutaminases - metabolism; IgA nephropathy; glomerulonephritis; inflammation; mucosal immunity

IgA1 complexes containing deglycosylated IgA1, IgG autoantibodies, and a soluble form of the IgA receptor (sCD89), are hallmarks of IgA nephropathy (IgAN). Food antigens, notably gluten, are associated with increased mucosal response and IgAN onset, but their implication in the pathology remains unk...