Published online before print December 28, 2007

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(American Journal of Pathology. 2008;172:31-36.)
© 2008 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2008.070131

Microbial IgA Protease Removes IgA Immune Complexes from Mouse Glomeruli In Vivo: Potential Therapy for IgA Nephropathy

Michael E. Lamm^*, Steven N. Emancipator^*, Janet K. Robinson^*, Michifumi Yamashita^*, Hisashi Fujioka, Jiazhou Qiu and Andrew G. Plaut

From the Departments of Pathology^*and Pharmacology,Case Western Reserve University, Cleveland, Ohio; and the Department of Medicine,Tufts-New England Medical Center, Boston, Massachusetts

The hallmark of IgA nephropathy (IgAN), the most common form of glomerulonephritis, is the presence of mesangial deposits containing IgA, specifically the IgA1 subclass, as the most prominent component. The deposited IgA is considered to be part of an immune complex. The family of enzymes known as bacterial IgA proteases exhibits substrate specificity that is essentially limited to the hinge region of IgA1. Here we demonstrate the ability of systemically administered IgA protease to remove glomerular IgA immune complexes, both the antigen and antibody components, in a passive mouse model of IgAN. Thus, IgA protease may have potential as a therapeutic agent for human IgAN.