Up-regulation of interleukin-4 and CD23/FcεRII in minimal change nephrotic syndrome
Up-regulation of interleukin-4 and CD23/FcεRII in minimal change nephrotic syndrome
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DOI：
10.1007/s004670050592
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发表时间：
1999-04-01
影响因子：
3
通讯作者：
Lee, CE
中科院分区：
文献类型：
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作者：
Cho, BS;Yoon, SR;Lee, CE
虽然儿童微小病变型肾病综合征（MCNS）的发病机制尚未明确界定，目前的假设有利于参与T细胞功能障碍。MCNS的症状发作和复发通常与过敏和血清IgE水平升高有关。由于T细胞衍生的细胞因子白细胞介素-4（IL-4）在调节IgE产生和过敏反应中起着关键作用，我们研究了IL-4在MCNS病理生理学中的作用。使用荧光激活细胞扫描，我们观察到一个显着较高的表达CD 23，II型IgE受体（Fc区RII），新鲜B细胞从活跃MCNS患者（n=22）与年龄匹配的健康正常对照组（n=12）相比。CD 23的上调与MCNS外周血淋巴细胞（PBL）培养上清液中IL-4活性高于有丝分裂原刺激的正常PBL相关，如PBL上清液对扁桃体B细胞的CD 23诱导作用所评估。此外，北方印迹和基于逆转录的聚合酶链反应分析显示，与健康正常人或患有其他肾脏疾病的疾病对照相比，在有丝分裂原刺激和未刺激的MCNS PBL中IL-4 mRNA水平显著升高。总之，这些结果强烈表明，T细胞中IL-4的上调可能是MCNS中涉及的T细胞功能障碍的一部分。
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 (Fc epsilon RII), 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.