Many forms of glomerulonephritis are mediated by autoimmunity. While autoantibodies are often pathogenic, cell-mediated immunity plays an important role in a number of forms of rapidly progressive glomerulonephritis. This unit describes the induction of cell-mediated autoimmune glomerular disease in mice. One disease model, experimental anti-glomerular basement membrane (GBM) disease, features autoreactivity to a well-defined component of type IV collagen found in the GBM, alpha3(IV)NC1. The other models the cell-mediated effector response in forms of renal vasculitis, where autoantibodies to myeloperoxidase result in systemic neutrophil activation, resulting in their localization to the glomerulus and the subsequent deposition of myeloperoxidase within glomerular capillaries. There, myeloperoxidase acts as a planted autoantigen and is recognized by effector autoreactive myeloperoxidase-specific T cells. These models are useful both in defining mechanisms germane to the development of autoimmunity to alpha3(IV)NC1 and myeloperoxidase, and in dissecting the role of cell-mediated responses in effecting glomerular injury. (c) 2014 by John Wiley Sons, Inc.