Molecular Insights into the Pathogenesis of IgA Nephropathy.
Paris, France. In Trends Mol Med, Dec 2015
To date, three key molecules have been implicated in IC formation, correlating with disease progression/recurrence after transplantation: galactose-deficient IgA1 (Gd-IgA1), IgG anti-Gd-IgA1 antibodies, and soluble CD89 (an Fc receptor for IgA).
Role of complement in IgA nephropathy.
Leiden, Netherlands. In J Nephrol, Dec 2015
This mesangial IgA has been found to consist mainly of polymeric IgA1 which drives the activation of the mesangial cells and results in excessive production of several inflammatory mediators.
New Insights into the Pathogenesis of IgA Nephropathy.
Birmingham, United States. In Kidney Dis (basel), May 2015
BACKGROUND: IgA nephropathy, a frequent cause of end-stage renal disease, is an autoimmune disease wherein immune complexes consisting of IgA1 with galactose-deficient O-glycans (autoantigen) and anti-glycan autoantibodies deposit in glomeruli and induce renal injury.
IgA nephropathy: molecular mechanisms of the disease.
Birmingham, United States. In Annu Rev Pathol, 2013
In patients with this disease, altered glycan structures in the unique hinge region of the heavy chains of IgA1 molecules lead to the exposure of antigenic determinants, which are recognized by naturally occurring antiglycan antibodies of the IgG and/or IgA1 isotype.