My research leverages my multi-disciplinary training in biochemistry, immunology and nephrology to elucidate the molecular mechanisms underlying the etiology and pathogenesis of antibody (Ab)-mediated glomerular diseases. I have extensive experience and expertise studying the biochemistry of type IV collagen of the glomerular basement membrane (GBM) and its role in Goodpasture disease (anti-GBM antibody nephritis) and Alport syndrome. My research has used the paradigm of Goodpasture disease to address the mechanisms eliciting abnormal immune responses against a345(IV) collagen and how the resulting anti-GBM Abs mediate glomerulonephritis. Overall, my work has elucidated the organization of Goodpasture autoantigen, providing the framework for understanding how tolerance to collagen IV is established in health and breached in anti-GBM disease. I have established how the assembly of a345(IV) collagen into quaternary structures hides cryptic B cell auto-epitopes while also creating new quaternary epitopes, thereby shaping immune tolerance and autoimmunity to collagen IV. My lab has also developed a robust mouse model faithfully recapitulate the clinical and morphologic hallmarks of human membranous nephropathy, in which subepithelial immune complexes induce severe albuminuria and nephrotic syndrome in a manner dependent on complement activation and the neonatal Fc receptor (FcRn). To further elucidate how human IgG autoAbs cause glomerular injury, I have recently developed a novel functional assay for complement activation by human autoAbs bound to their target antigen, which provide a model for glomerular immune complexes. In summary, I have established a strong track record of successful, productive, innovative and collaborative research in the area of Ab-mediated kidney disease.