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Analysis of Signal Transduction in Immunocompetent Cells by Protein Phosphatase and its Application for Autoimmune Disease

蛋白磷酸酶在免疫活性细胞中的信号转导分析及其在自身免疫性疾病中的应用

基本信息

批准号：
02454152
负责人：
KIKUCHI Kunimi
金额：
$ 3.71万
依托单位：
Hokkaido University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1991
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-02454152/
关键词：
Protein Phosphatase MRL lpr Mice Spleen Thymus PP1 PP2A PP2C Signal Transduction T細胞 B細胞分別定量

项目摘要

The differential assay conditions for protein phoshatases PP1, PP2A and PP2C were extensively studied by using crude extracts from mouse lymphoid tissues as enzyme sources. Under these conditions, the protein phosphatase activities were measured in MRL/lpr mice, autoimmune prone mice, and the control. In MRL/lpr mice, significant alterations in protein phosphatase activities were demonstrated. In spleen and liver from MRL/lpr mice, activities of PP1 and PP2A were distinctively elevated than those of the control mice. The increases in PP2A activity of MRL/lpr spleen and liver were taken to be due to accumulation of the abnormal lymphocytes emerged in MRL/lpr mice. Although the PP1 activity in MRL/lpr lymph nodes was nodes lower than those of normal spleen and thymus, it was greatly increased by Co^<2+>-trypsin treatment so that the PP1 activity of MRL/lpr lymph nodes was the highest among those all the tissues examined. In contrast, PP2C activities showed no remarkable alterations in the autoimmune disease model mice. Then, the protein phosphatase activities were measured by using T, B, Mphi cells prepared from mouse lymphoid tissues, and the alterations in PP1 activity was also confirmed. These results demonstrated a specific elevation in potency of protein dephosphorylation in the tissues with this disease, a new possibility to explain the defect in signal transduction in the MRL/lpr mice.

以小鼠淋巴组织粗提物为酶源，广泛研究了蛋白磷酸酶PP1、PP2A和PP2C的差异测定条件。在这些条件下，测量了MRL/lpr小鼠、自身免疫易感性小鼠和对照组的蛋白磷酸酶活性。在MRL/lpr小鼠中，蛋白磷酸酶活性发生了显著变化。在MRL/lpr小鼠的脾脏和肝脏中，PP1和PP2A的活性明显高于对照组。MRL/lpr小鼠脾脏和肝脏中PP2A活性的升高被认为是由于MRL/lpr小鼠中出现的异常淋巴细胞的积累。虽然MRL/lpr淋巴结的PP1活性低于正常脾脏和胸腺，但Co^<2+>-胰蛋白酶处理后PP1活性显著升高，使MRL/lpr淋巴结的PP1活性在所有检查组织中最高。相比之下，PP2C活性在自身免疫性疾病模型小鼠中没有显着改变。然后用小鼠淋巴组织制备的T、B、Mphi细胞测定蛋白磷酸酶活性，并证实PP1活性的变化。这些结果表明，在患有这种疾病的组织中，蛋白质去磷酸化的效力特异性升高，这是解释MRL/lpr小鼠信号转导缺陷的一种新的可能性。