Our understanding of the role of the immune system in modulating glomerular injury continues to evolve. The participation of antibody, complement, and neutrophils alone cannot completely explain many aspects of the pathways of experimental and human glomerulonephritis. The elements of the immune system that mediate cellular immunity, T lymphocytes and monocytes, also appear to be important effectors of glomerulonephritis. An understanding of the role of cell-mediated immunity in renal disease is essential in designing therapies to interrupt immunologically sustained glomerular damage.