ERK在ALR抑制免疫过程中的变化及意义  

Variation and function of ERK in ALR-mediated immunosuppression

作　　者：王新国[1] 刘杞[1] 孙航[1] 谢松丽[1] 梁珊[1] 彭明利[1] 陈学华[1] 

机构地区：[1]重庆医科大学病毒性肝炎研究所教育部感染性疾病分子生物学重点实验室,400010

出　　处：《免疫学杂志》2010年第2期128-131,共4页Immunological Journal

基　　金：国家自然科学基金(30570826);重庆市自然科学基金(CSTC2008BB5228)

摘　　要：目的观察肝再生增强因子(ALR)对外周血单核细胞增殖时ERK的影响,以探明ALR免疫抑制相关机理。方法梯度离心法分离健康人外周单核细胞,用ConA 5μg/ml刺激细胞增殖,选定最佳研究时间;观察不同剂量ALR抑制功能,选用最佳抑制剂量;利用Western blot检测ALR抑制细胞增殖时ERK的磷酸化改变。结果 ConA刺激细胞增殖最佳时间是60 h,ALR能抑制细胞增殖,并呈剂量依赖关系,30μg/ml ALR抑制效果最显著;ALR对单核细胞无直接增殖作用。ConA能引起ERK含量和磷酸化明显增加,ALR则抑制ConA对ERK的刺激,以抑制ERK2最明显。结论 ALR可能通ERK的含量和抑制ERK2的磷酸化抑制细胞增殖。Augmenter of liver regeneration （ALR） can promote proliferation of hepatocytes, as well as plays as an immunologic suppressor factor. The study aims to investigate the effects of ALR on the expression and function of ERKS in the PBMC proliferation and evaluate the relevant mechanism. PBMCs were isolated from healthy volunteers by gradient centrifugation. While a series of time and concentration of ALR were administrated for optimizing the time for cells proliferation stimulated with ConA （5 ug/ml） and the ALR dose to inhibit cell proliferation. The ERK and its phosphorylation degree were evaluated by Western blot. The optimal time for ConA stimulating proliferation was 60 h, and the optimal dose of ALR to inhibit cell proliferation was 30 ug/ml. And ALR inhibited cells proliferation in a dose-dependent manner. But ALR did not stimulate monocytes to proliferate. The ConA increased the content and phosphorylation of ERK significantly, but these increases were inhibited by ALR, especially the phosphorylation of ERK2. All these results suggest that ALR can inhibit the proliferation of PBMCs, probably by decreasing the total content of ERK and phosphorylation of ERK2.

关 键 词：肝再生增强因子(ALR) ERK 外周血单核细胞 免疫抑制 

分 类 号：R392.1[医药卫生—免疫学]