The involvement of immunoglobulin and complement in glomerulonephritis has been recognized for many decades, but the involvement of sensitized T cells and the contributions of cellular immunity have only recently been appreciated. The relative contributions of humoral and cellular immunity in the immunopathogenesis may be an important determinant of the various histological patterns and clinical features of human glomerulonephritis. Subsets of T helper cells, Th1 and Th2, induce immune activation with distinct patterns of involvement of immunoglobulin isotypes and cellular immune effectors. The relative activation of Th subsets is determined by a variety of factors including the nature, dose and mode of presentation of antigens and the cytokine milieu. The balance of Thl/Th2 activation may be important in directing effector pathways and patterns of injury in glomerulonephritis. In the effector phase, T cells are most prominent in proliferative and crescentic glomerulonephritis, where they are usually associated with other mediators of delayed-type hypersensitivity including macrophages and fibrin. In anti-neutrophil cytoplasmic antibody-associated crescentic glomerulonephritis, T cells are invariable participants, frequently in the absence of glomerular antibody deposition. In these forms of glomerulonephritis, which characteristically have a rapid course and poor outcome, T cells are likely to play a pivotal effector role.