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Mouse Models for Graft Arteriosclerosis

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Published on: May 14, 2013

干扰素玛受体缺陷小鼠的致命自身免疫性心肌炎:由于诱导性氧化合成酶诱导功能受损,增加了疾病的严重程度.

U Eriksson¹, M O Kurrer, R Bingisser

¹Medical Intensive Care Unit, University Hospital, Basel, Switzerland. klinerr@usz.unizh.ch

|January 4, 2001

概括

干扰素- (IFN-) 通过促进氧化的产生,防止致命的自身免疫性心肌炎. 这种细胞因子降低T细胞的反应,防止老鼠的持续性心脏炎症.

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科学领域:

免疫学免疫学免疫学
心血管研究研究心血管研究
自免疫性疾病自免疫性疾病

背景情况:

干扰素- (IFN-) 是调节炎症反应的关键细胞因子.
它在炎症性心脏病中的特定作用在很大程度上仍未被探索.

研究的目的:

研究IFN-在自身免疫性心肌炎中的作用.
阐明IFN-玛影响心脏炎症和T细胞反应的机制.

主要方法:

使用了IFN-马受体缺乏 (IFN-马R(-/-)) 和野生型小鼠,用心脏肌酸胺免疫.
评估心肌炎的严重程度,死亡率,T细胞反应和氧化合成酶 (NOS) 表达.
给野生类型的小鼠服用一个NOS抑制剂.

主要成果:

IFN-gammaR(-/-) 的小鼠患有严重的,持久的心肌炎,死亡率高.
野生类型的小鼠显示疾病的解决,而缺乏的小鼠显示持续的炎症.
在IFN-gammaR(-/-) 小鼠中观察到氧化的产生受损和CD4 T细胞的增多.
在野生型小鼠中,NOS抑制加剧了T细胞的增殖,并阻止了心肌炎的愈合.

结论:

IFN-在自身免疫性心肌炎中起着保护作用.
这种保护是通过诱导可诱导的氧化合成酶 (iNOS) 来实现的.
IFN-马信号降低了T细胞的反应,有助于疾病的解决.