Elevation of interleukin-4 and CD23(FcεRII) expression in idiopathic nephrotic syndromes

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Elevation of interleukin-4 and CD23(FcεRII) expression in idiopathic nephrotic syndromes
Suk Ran Yoon; S Y Kim; Choong Eun Lee; B S Cho; Kwang Ho Pyun
Bibliographic Citation
Korean Journal of Biological Response Modifiers, vol. 1, no. 1, pp. 125-131
Publication Year
Idiopathic nephrotic syndrome (INS), accompanied by massive loss of protein through glomerular membrane, is often referred to be associated with immune dysfunction. The elevated serum IgE levels and atopic symptoms have been frequently observed in these patients. We investigated the role of interleukin4 (IL4)in the pathogenesis of INS through the regulation of membrane FceRII, CD23(low affinity IgE receptor) on B cells. Substantially higher levels of CD23 expression were observed on freshly isolated nephrotic B cells (n=18)than normal B cells (n=10)as analyzed by fluorescence activated cell scanner (FACScan) using double antibody staining with anti Leu 16 (pan B marker)-FITC and anti Leu 20 (CD23)-PE. Sera from these patients also demonstrated an increased II,4 activity as compared with tho沈 from normal than normal T cells (up to 9 fold), as assessed by tonsillar B cell proliferation with anti p and CD23 expression. However, the responsiveness of nephrotic B cells to exogenously added IL-4(5-200u/ml) was similar to that of normal counterparts. As in the case of normal cells, interferon-ydFN-y) (lOO-lOOOu/ml) effectively inhibited the IL-4 induced CD23 expression by nephrotic B cells (up to 80% inhibition). It was noteworthy that nephrotic decrease in CD23 expression. These results suggest that INS is a T cell disorder involving abnormal production of IL-4 and that regulation of CD23 by IL-4 may play a role in the pathogenesis of INS.
Korea Soc-Assoc-Inst
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Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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