Defective cell-mediated immunity in lipoid nephrosis.
Defective cell-mediated immunity in lipoid nephrosis.
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类脂性肾病中细胞介导的免疫缺陷。
DOI：
10.1159/000233501
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
M. Hatano
中科院分区：
文献类型：
--
作者：
K. Matsumoto;K. Osakabe;H. Katayama;K. Okano;M. Hatano
本文对28例经活检证实的类脂质肾病（LN）患者进行了细胞免疫（CMI）研究。LN合并肾病综合征（NS）患者的CMI明显降低，表现为皮肤对纯化蛋白衍生物（PPD）的迟发超敏反应减弱，局部移植物抗宿主反应（GVHR）降低，T淋巴细胞比例降低，淋巴细胞转化植物血凝素（PHA）能力减弱。与正常人相比，伴NS的LN患者伴刀豆球蛋白A（Con A）诱导的抑制细胞活性（SCA）显着增加。相反，在缓解期LN患者和慢性系膜增生性肾小球肾炎（CGN）患者中研究的CMI和SCA的平均水平与正常受试者没有差异。我们的研究结果支持这样的观点，至少在一些LN患者的NS，激活抑制细胞的存在，并可能占其降低CMI。
Cell-mediated immunity (CMI) was studied in 28 patients with biopsy-proven lipoid nephrosis (LN). The LN patients with nephrotic syndrome (NS) had a significant depression in CMI, characterized by impaired delayed hypersensitivity skin reactivity to purified protein derivative (PPD), depressed local graft-versus-host reaction (GVHR), decreased proportion of T lymphocytes and diminished lymphocyte transformation to phytohemagglutinin (PHA). Concanavalin A (Con A)-induced suppressor cell activity (SCA) was found to be significantly increased in LN patients with NS compared to that in normal individuals. In contrast, the mean levels of CMI and SCA studied in LN patients in remission and in patients with chronic mesangial proliferative glomerulonephritis (CGN) did not differ from normal subjects. Our findings support the notion that at least in some LN patients with the NS, activated suppressor cells are present and possibly account for their decreased CMI.