It has been suggested that the immune system is involved in the development of lipoid nephrosis. The aim of the study was to estimate whether an elevated serum concentration of soluble interleukin-2 receptor (sIL-2R) is caused by increased expression of IL-2 receptors on the surface of lymphocytes T (CD3+CD25+). 20 children with lipoid nephrosis and 15 healthy children served as control were evaluated. T cell subpopulations were assayed with flow cytometry, using monoclonal antibodies. The concentration of sIL-2R was determined by enzyme-linked immunosorbent assay (ELISA). The patients with lipoid nephrosis had elevated serum levels of sIL-2R compared with healthy controls. Although the subpopulation of T cell CD3+CD25+ was decreased in nephrotic children. These results could testify against direct contribution of T cell immune response in the pathogenesis of lipoid nephrosis.
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