白细胞介素-1受体拮抗剂表达异常的转基因小鼠对胶原诱导性关节炎的易感性改变。
Altered susceptibility to collagen-induced arthritis in transgenic mice with aberrant expression of interleukin-1 receptor antagonist.
作者信息
Ma Y, Thornton S, Boivin G P, Hirsh D, Hirsch R, Hirsch E
机构信息
Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
出版信息
Arthritis Rheum. 1998 Oct;41(10):1798-805. doi: 10.1002/1529-0131(199810)41:10<1798::AID-ART11>3.0.CO;2-L.
OBJECTIVE
To determine the effect of overexpression or deletion of interleukin-1 receptor antagonist (IL-1Ra) in collagen-induced arthritis (CIA).
METHODS
Mice overexpressing the IL-1Ra gene under the control of its endogenous promoter, mice lacking IL-1Ra, and normal littermate controls were immunized with bovine type II collagen (CII) and compared in terms of features of CIA.
RESULTS
Mice overexpressing IL-1Ra had a significant reduction in the incidence and severity of CIA. After CII immunization, IL-1Ra messenger RNA was overexpressed in the spleens, but not in the paws, of transgenic mice. Minimal differences were observed in the humoral or cellular immune responses to CII. Mice lacking IL-1Ra had a significantly earlier onset of CIA, with increased severity.
CONCLUSION
Endogenous expression of IL-1Ra is a critical determinant of susceptibility to CIA. These findings suggest potential therapeutic interventions for autoimmune arthritis.
目的
确定白细胞介素-1受体拮抗剂（IL-1Ra）过表达或缺失对胶原诱导的关节炎（CIA）的影响。
方法
以内源性启动子控制下过表达IL-1Ra基因的小鼠、缺乏IL-1Ra的小鼠以及正常同窝对照小鼠用牛II型胶原（CII）进行免疫，并在CIA特征方面进行比较。
结果
过表达IL-1Ra的小鼠CIA的发病率和严重程度显著降低。CII免疫后，转基因小鼠脾脏中IL-1Ra信使核糖核酸过表达，但爪中未过表达。在对CII的体液或细胞免疫反应中观察到极小差异。缺乏IL-1Ra的小鼠CIA发病明显更早，严重程度增加。
结论
IL-1Ra的内源性表达是对CIA易感性的关键决定因素。这些发现提示了自身免疫性关节炎的潜在治疗干预措施。
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