• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Role for interferon-gamma in rat strains with different susceptibility to experimental autoimmune myasthenia gravis.
【24h】

Role for interferon-gamma in rat strains with different susceptibility to experimental autoimmune myasthenia gravis.

机译：γ干扰素在对实验性自身免疫性重症肌无力有不同敏感性的大鼠品系中的作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Experimental autoimmune myasthenia gravis (EAMG) is caused by autoantibodies against the nicotinic acetylcholine receptor (AChR) at the neuromuscular postsynaptic membrane and represents an animal model of myasthenia gravis in human. Recent studies highlighted the roles of TH1 cytokines (IFN-gamma, IL-12), rather than TH2 cytokines (IL-4), in the pathogenesis of EAMG by using homozygous (-/-) knockout mice with an EAMG-susceptible genetic background. To further evaluate a role for IFN-gamma, we injected recombinant rat IFN-gamma (rrIFN-gamma) at the time of immunization with AChR in complete Freund's adjuvant to EAMG-susceptible Lewis rats and EAMG-resistant Wistar Furth (WF) rats. RrIFN-gamma enhanced Lewis rat EAMG. The exacerbated muscular weakness was associated with higher levels of anti-AChR IgG and enhanced TNF-alpha responses. Anti-AChR IgG antibody levels were augmented to a similar extent as in Lewis rats, however, the identical immunization and IFN-gamma injection induced only mild and transient EAMG in WF rats due to the default TH3 phenotype development and inherent low TH1 responses. We conclude that IFN-gamma plays a major role in the pathogenesis of EAMG in the Lewis rat, but fails to break disease resistance in the WF rat. Copyright 2000 Academic Press.
机译：实验性自身免疫性重症肌无力（EAMG）是由针对神经肌肉突触后膜的烟碱乙酰胆碱受体（AChR）的自身抗体引起的，代表了人类重症肌无力的动物模型。最近的研究通过使用具有EAMG易感基因背景的纯合（-/-）基因敲除小鼠，突出了TH1细胞因子（IFN-γ，IL-12）而不是TH2细胞因子（IL-4）的作用。 。为了进一步评估IFN-γ的作用，我们在AChR免疫时注射了重组大鼠IFN-γ（rrIFN-γ），作为对EAMG易感Lewis大鼠和EAMG抗性Wistar Furth（WF）大鼠的完全弗氏佐剂。 RrIFN-γ增强了Lewis大鼠EAMG。加剧的肌无力与较高水平的抗AChR IgG和增强的TNF-α反应有关。抗AChR IgG抗体的水平增加到与Lewis大鼠相似的程度，但是，由于默认的TH3表型发育和固有的低TH1反应，相同的免疫和IFN-γ注射仅在WF大鼠中诱导了轻度和短暂的EAMG。我们得出结论，IFN-γ在Lewis大鼠的EAMG发病机理中起主要作用，但未能破坏WF大鼠的抗病性。版权所有2000学术出版社。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号