摘要
通过建立大鼠佐剂性关节炎(AA)动物模型,研究了IL-10和IL-1ra对正常及AA大鼠腹腔Mφ分泌细胞因子的调节作用,并利用分子杂交技术在基因水平上对其作用机制进行了初步探讨。结果表明:AA大鼠腹腔Mφ呈高度活化状态,产生大量炎症细胞因子IL-1、IL-6、IL-8和TNF等,IL-10和IL-1ra对正常及AA大鼠腹腔Mφ细胞因子的产生均呈显著抑制作用,并呈剂量依赖关系。IL-10和IL-1ra具有协同抑制作用。进一步研究发现IL-10和IL-1ra能抑制LPS诱导的腹腔MφIL-8mRNA表达,表明其抑制作用发生在基因水平上。提示IL-10和IL-1ra是有效的免疫抑制剂。
In this paper we studied the immunomodulatory effects and its mechanisms of IL 10 and IL 1 receptor antagonist (IL 1ra) on cytokine production from peritoneal macrophages in normal and AA rats. The results showed that peritoneal macrophages in AA rats could secrete more substantial IL 1,IL 6,IL 8 and TNF than those in normal rats. IL 10 and IL 1ra significantly down regulated cytokine production from peritoneal macrophages in normal and AA rats, which were dose dependent. Furthermore IL 10 and IL 1ra had synergistic inhibitory effect. Dot Blot revealed that IL 10 and IL 1ra could dramatically reduced IL 8 mRNA expression from peritoneal macrophages in normal rats. In conclusion, IL 10 and IL 1ra were potent inhibitors in immunoresponses, which can provide valuble theoretical and experimental evidence for its clinical applications to anti inflammation.
出处
《免疫学杂志》
CAS
CSCD
北大核心
1996年第3期165-168,共4页
Immunological Journal
关键词
白细胞介素10
IL-1RA
腹腔
巨噬细胞
免疫调节
IL 10,IL 1ra, Rat peritoneal macrophage, Immunoregulation, Nucleic acid hybridization