Study of the Role of T-regulatory Lymphocytes in the Pathogenesis of Idiopathic Nephrotic Syndrome in Children

Abstract

he hallmark of idiopathic nephrotic syndrome (INS) is massive proteinuria leading to decreased circulating albumin levels. The initiative event that produces proteinuria remains unknown (Lai et al., 2007). Circulating T cells were postulated to release cytokines that reached the glomerulus and induced an increase in permeability to plasma proteins. Indirect evidence for this hypothesis was supported by the absence of humoral (immunoglobulins and complement) components in glomeruli, the often prompt response to treatment with agents known to inhibit T cell function (corticosteroids, cyclosporine, cyclophosphamide, mycophenolate), the association of remission following measles infection (which is known to depress T cell immunity), and the association with T cell disorders, such as Hodgkin’s lymphoma (Karle et al., 2002). In a study which tested the hypothesis that, in MCNS, the Treg cell suppressor mechanism is deficient, thereby allowing the T helper cells, after stimulation, to secrete excessive amounts of cytokines, they found persistence of the proposed pathogenic cytokines and concluded that the impaired Treg cell function in these patients may have pathogenetic and therapeutic implications (Bonilla-Felix et al., 1999). In our follow up case-control study, 20 patients with newly diagnosed idiopathic nephrotic syndrome in the Pediatric Nephrology Clinic, Children’s Hospital, Ain Shams University during the period between January 2011 and January 2013 were T