L ittle is known about the potential role of T cells in the inflammatory renal disease glomerulonephritis (GN). GN has been historically viewed as a product of immune complex–mediated complement activation, and the presence of autoantibodies made identifying T cell–specific effector contributions difficult to elucidate. In this issue of the JCI, Heymann et al. generate what they believe to be a novel, transgenic murine model of GN, demonstrating a direct role for CD8⁺ T cells, activated CD4⁺ T cells, and DCs in the pathogenesis of GN (see the related article, doi:10.1172/JCI38399).