Advisory Committee Chair
Jan Novak
Advisory Committee Members
Susan Bellis
Rodney King
Matthew B Renfrow
Dana Rizk
Document Type
Dissertation
Date of Award
2023
Degree Name by School
Doctor of Philosophy (PhD) College of Arts and Sciences
Abstract
IgA nephropathy (IgAN) is an autoimmune disease that is the most common form of glomerulonephritis in the world, and results in end-stage renal disease in 40% of patients. In IgAN, human immunoglobulin A1 (IgA1) has reduced levels of galactose (Gal) in the IgA1 O-glycosylated hinge region (HR) known as Gal deficient IgA1 (Gd-IgA1). These Gd-IgA1 glycoforms, which are elevated in circulation of IgAN patients, are recognized by Gd-IgA1-specific IgG autoantibodies, resulting in the formation of pathogenic immune complexes (CICs). Some of these CICs accumulate in the mesangium of glomeruli and induce kidney injury. Although the link between these deposits and the clinical manifestations of IgAN are established, there remains a gap in knowledge about the which glycoforms of IgA1 contribute to IgAN pathogenesis. The exact molecular origin of these Gd-IgA1 glycoforms in pathogenic CICs remains unknown as IgA1 exist in three distinct molecular forms: monomeric (produced by bone marrow 80-90% of total serum IgA1) (mIgA1), polymeric (produced by mucosal tissues 10-20% of total IgA1) (pIgA1), IgA1 bound in CICs (
Recommended Citation
Craine, Ellenore P., "Molecular Phenotyping of Serum IgA1 0-Glycoforms in the Context of IgA Nephropthy" (2023). All ETDs from UAB. 39.
https://digitalcommons.library.uab.edu/etd-collection/39