A regulatory system for soluble immune response suppressor production in steroid-responsive nephrotic syndrome.

A regulatory system for soluble immune response suppressor production in steroid-responsive nephrotic syndrome.
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类固醇反应性肾病综合征中可溶性免疫反应抑制因子产生的调节系统。

DOI:
10.1038/ki.1990.180
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发表时间:
1990
影响因子:
19.6
通讯作者:
Schnaper,HW
Schnaper,HW
中科院分区:
医学1区
文献类型:
--
作者:
Schnaper,HW

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类固醇反应性肾病综合征中可溶性免疫反应抑制因子产生的调控系统。肾病综合征患者的免疫反应经常受到抑制。以前,已经确定类固醇反应性肾病综合征(SRNS)的受试者产生淋巴因子,可溶性免疫反应抑制因子(SIRS)。本实验探讨了抑制细胞激活的潜在途径。SRNS患者的血清刺激正常CD8+淋巴细胞产生SIRS。用蛋白酶K或煮沸处理可使血清sirs诱导活性消失,但透析、酸化至pH 2或加热至56°C均不影响血清sirs诱导活性。该血清因子在功能和抗原性上可与SIRS和干扰素α或IFNγ区分开来。培养的患者淋巴细胞富集CD4+细胞的上清液也能激活正常的CD8+淋巴细胞产生SIRS。淋巴细胞来源的活性表现出与血清因子相似的特征。凝胶过滤层析法估计这两种因子的分子量为13000至18000道尔顿,用反相高效液相色谱法对同一患者的血清和淋巴细胞上清液的活性进行了类似的洗脱。这些数据表明,血清SIRS诱导活性来源于抑制诱导剂淋巴细胞,并表明在类固醇反应性肾病患者中存在SIRS产生的调节机制。
A regulatory system for soluble immune response suppressor production in steroid-responsive nephrotic syndrome. Patients with nephrotic syndrome frequently have suppressed immune responses. Previously, it has been determined that subjects with steroid-responsive nephrotic syndrome (SRNS) produce the lymphokine, soluble immune response suppressor (SIRS). In the present group of experiments, a potential pathway of suppressor cell activation was investigated. Sera from patients with SRNS stimulated normal CD8+lymphocytes to produce SIRS. Serum SIRS-inducing activity was abrogated by treatment with proteinase K or boiling, but was not affected by dialysis, acidification to pH 2, or heating to 56°C. This serum factor could be distinguished functionally and antigenically from SIRS and from interferon (IFN)αor IFNγ. Supernatants of cultured patient lymphocytes enriched for CD4+cells were also found to activate normal CD8+lymphocytes to produce SIRS. The lymphocyte-derived activity showed similar characteristics to those of the serum factor. Molecular weight of both factors was estimated to be 13,000 to 18,000 daltons by gel filtration chromatography, and activity of serum and lymphocyte supernatant from the same patients eluted with similar patterns on reversed-phase HPLG. These data suggest that serum SIRS-inducing activity is derived from a suppressor-inducer lymphocyte, and indicate the presence of a regulatory mechanism for SIRS production in steroid-responsive nephrotic patients.
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DOI: --
发表时间: 1984
期刊: The Journal of biological chemistry
影响因子: --
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DOI: --
发表时间: 1986
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