title: Studies on the role of interleukin-4 and Fc epsilon RII in the pathogenesis of minimal change nephrotic syndrome.
abstract: Childhood minimal change nephrotic syndrome (MCNS) has often been associated with allergic symptoms such as urticaria, bronchial asthma, atopic dermatitis, allergic rhinitis and elevated IgE levels and referred to involve immune dysfunction. Fc epsilon RII is known to be involved in IgE production and response. Interleukin-4 is being recognized as a major cytokine up-regulating IgE production. Hence the present study is aimed at investigating the role of interleukin-4 and Fc epsilon RII in the pathogenesis of MCNS. IgE was measured by ELISA. Fc epsilon RII was analyzed by fluorescence activated cell scanner (FAC-scan) by double antibody staining with anti Leu16-FITC and anti Leu20-PE. Soluble IgE receptor was measured by ELISA using anti CD23 antibody (3-5-14). Interleukin-4 activities were measured by CD23 expression on purified human tonsillar B cells. Serum IgE levels were significantly higher in MCNS (1,507 +/- 680 IU/dl) than in normal controls (123 +/- 99.2 IU/dl). A significantly higher expression of membrane Fc epsilon RII was noted for MCNS (41 +/- 12%) than that in normal controls (18 +/- 6.2%) (p < 0.001). Soluble CD23 levels were also significantly higher in MCNS (198 +/- 39.3%) than in normal controls (153 +/- 13.4) (p < 0.01). Interleukin-4 activity in sera of MCNS (12U/ml) was also significantly higher than normal controls (4.5U/ml). These results indicate that increased production of Fc epsilon RII and interleukin-4 may play an important role in the pathogenesis of MCNS.
authors.affiliation: Department of Pediatrics, College of Medicine, Kyung Hee University, Seoul, Korea.
authors.forename: B S
authors.initials: BS
authors.lastname: Cho
authors.forename: C E
authors.initials: CE
authors.lastname: Lee
authors.forename: K H
authors.initials: KH
authors.lastname: Pyun
mesh_terms: D001402:B-Lymphocytes / Q000276:immunology; D002648:Child; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D015847:Interleukin-4 / Q000502:physiology*; D009402:Nephrosis, Lipoid / Q000209:etiology* / Q000503:physiopathology; D017455:Receptors, IgE / Q000096:biosynthesis / Q000502:physiology*; D012995:Solubility
chemical_list: D017455:Receptors, IgE; D015847:Interleukin-4; D007073:Immunoglobulin E