Childhood minimal change nephrotic syndrome (MCNS)is often associated with hyper-sensitivity reactions and considered to be caused by immune dysfunction. The elevated serum IgE levels and atopic symptoms have been frequently associated in these patients. The present therapy for MCNS mainly depends on corticosteroids, alkylating agents such as chlorambucil, cyclophosphamide and cyclosporin A (Cy, A). However, frequent relapses and severe side effects caused by such therapy necessitate development of a more specific and effective therapeutic regimen.Recently, a T cell derived cytokine, interleukin 4 (IL-4)is being recognized as a major cytokine up-regulating IgE production and response, while interferon- (IFN- )counteracts IL-4 actions to down-regulate the IL-4 induced IgE response. Hence, the present study is aimed to investigate the role of IL-4 in MCNS. Using freshly isolated peripheral blood from active MCNS patients and normal controls, it was found that not only serum IgE levels, but also membrane-bound IgE receptor expression and soluble IgE receptor production were also significantly higher in MCNS than in mormal controls, which in turn correlated well with the increased IL-4 activities in the patients' sera. Interestingly among MCNS patients receiving a steroid therapy, those who responded with a clinical remission demonstrated a noticeable decrease in IgE receptor levels on their B cells. From these results it is concluded that MCNS is highly associated with not only increased serum IgE, but also elevated IL-4 activities and IgE receptor expression. In addition, IgE receptor could be a good prognostic marker in MCNS.
Adrenal Cortex Hormones ; Alkylating Agents ; B-Lymphocytes ; Chlorambucil ; Cyclophosphamide ; Cyclosporine ; Humans ; Immunoglobulin E ; Interleukin-4 ; Nephrosis, Lipoid* ; Recurrence