Circulating immune complexes [1], in situ complexes and antibodies to the basement membrane [2, 3] have been involved in the pathogenesis of some forms of glomerular disease. However, in the complex defined as idiopathic nephrotic syndrome (INS), there is a paucity of evidence to support classical immunological mechanisms. The morphological lesions seen in this complex consist of minimal change, mesangial hypercellularity IgM nephropathy and focal segmental sclerosis (fig. 1). Transition from either minimal change or mesangial hypercellularity and IgM nephropathy frequently occurs in patients with a relapsing pattern of nephrotic syndrome [4, 5], suggesting that the disease process has a broad but continuing spectrum. The morphological transition also suggests that similar stimuli are operating in the genesis of the various identified forms of INS. The scarcity of immune deposition in INS leads to the suggestion that the altered glomerular permeability is a reflection of changes in T cell function [6]. Soon after Shalhoub's hypothesis in 1974 a variety of lymphokines were identified in patients with INS. In 1974 Ooi et al.[7] observed a circulating factor designated as lymphocytoxin in patients with INS, next in 1975 Lagrue et al.[8] identified the presence of a lymphokine in the supernatant of serum taken from patients with INS. In 1976, using a leukocyte migration test Eyres et al.[9] demonstrated that patients with INS have evidence of T cell sensitization. In 1979 Moorthy et al.[10] showed that plasma from INS patients inhibited autologous lymphocyte response to mitogen stimulation. In 1982, Fodor et al.[11] observed that in INS patients there is a reduction in the blast transformation of lymphocytes when stimulated with a mitogen. In 1984, Schnaper et al.[12] identified a factor in the serum of INS patients which they labeled soluble immune response suppressor.