Up-regulation of interleukin-4 and CD23/FcepsilonRII in minimal change nephrotic syndrome

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Title
Up-regulation of interleukin-4 and CD23/FcepsilonRII in minimal change nephrotic syndrome
Author(s)
B S Cho; Suk Ran Yoon; J Y Jang; K H Pyun; C E Lee
Bibliographic Citation
Pediatric Nephrology, vol. 13, no. 3, pp. 199-204
Publication Year
1999
Abstract
Although the pathogenesis of childhood minimal change nephrotic syndrome (MCNS) has not been clearly defined, the current hypothesis favors an involvement of T cell dysfunction. The symptom onset and the relapse of MCNS are frequently associated with allergy and increased IgE levels in sera. Since a T cell-derived cytokine interleukin-4 (IL-4) plays a key role in the regulation of IgE production and allergic response, we investigated the role of IL-4 in the pathophysiology of MCNS. Using fluorescence-activated cell scanning we observed a significantly higher expression of CD23, the type II IgE receptor (FcepsilonRII), on fresh B cells from active MCNS patients (n=22) compared with age-matched healthy normal controls (n=12). The upregulation of CD23 correlates with greater IL-4 activity in the culture supernatant of MCNS peripheral blood lymphocytes (PBLs) than normal PBLs stimulated by mitogens, as assessed by the CD23-inducing effect of the PBL supernatant on tonsillar B cells. Furthermore, Northern blot and reverse transcription-based polymerase chain reaction analysis have revealed significantly elevated levels of IL-4 mRNAs both in mitogen-stimulated and unstimulated MCNS PBLs, compared with healthy normals or disease controls with other renal disorders. Together these results strongly suggest that the upregulation of IL-4 in T cells may be part of the T cell dysfunction involved in MCNS.
Keyword
Minimal change nephrotic syndromeType II IgE receptorInterleukin-4Interleukin-4 mRNAUpregulation&
ISSN
0931-041X
Publisher
Springer
DOI
http://dx.doi.org/10.1007/s004670050592
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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