Holmdahl R, Jansson L, Meyerson B, Klareskog L
Department of Medical and Physiological Chemistry, University of Uppsala, Sweden.
Clin Exp Immunol. 1987 Nov;70(2):372-8.
Experimental animal models can be used to help understand how oestrogen modulates autoimmune arthritis. We have previously shown that castration of female DBA/1 mice exaggerates arthritis induced with type II collagen. This report shows that treatment of castrated DBA/1 mice with low doses (0.2 micrograms twice a week) of beta-oestradiol reduces the incidence (37% vs 78% in controls) and severity (3.9 vs 5.6 mean scores) of arthritis. Levels of IgG anti type II collagen antibodies are decreased whereas levels of IgM antibodies are increased in the beta-oestradiol treated mice. The T cell response, as measured by a 3H-thymidine assay, is reduced in the beta-oestradiol treated mice. The results suggest that treatment with low doses of beta-oestradiol exerts a suppressive effect on both development of collagen arthritis as well as T cell dependent immune reactivity towards type II collagen.
实验动物模型可用于帮助理解雌激素如何调节自身免疫性关节炎。我们之前已经表明,雌性DBA/1小鼠去势会加剧由II型胶原诱导的关节炎。本报告显示,用低剂量(每周两次,每次0.2微克)的β-雌二醇治疗去势的DBA/1小鼠,可降低关节炎的发病率(37% 对比对照组的78%)和严重程度(平均评分3.9对比5.6)。在接受β-雌二醇治疗的小鼠中,抗II型胶原IgG抗体水平降低,而IgM抗体水平升高。通过3H-胸腺嘧啶核苷测定法测量,接受β-雌二醇治疗的小鼠的T细胞反应降低。结果表明,低剂量β-雌二醇治疗对胶原性关节炎的发展以及针对II型胶原的T细胞依赖性免疫反应均具有抑制作用。