• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Role of T Cells and Gamma Interferon during Induction of Hypersensitivity to Lipopolysaccharide by Toxic Shock Syndrome Toxin 1 in Mice
【24h】

Role of T Cells and Gamma Interferon during Induction of Hypersensitivity to Lipopolysaccharide by Toxic Shock Syndrome Toxin 1 in Mice

机译：T细胞和γ干扰素在毒性休克综合征毒素1对小鼠脂多糖超敏性诱导中的作用

获取原文
       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The superantigenic function of toxic shock syndrome toxin 1 (TSST-1) is generally regarded as an important determinant of its lethal effects in humans or experimental animals. This study examined the role of superantigenicity in a BALB/c mouse model of lethal TSST-1-induced hypersensitivity to lipopolysaccharide (LPS). In this model, TSST-1 greatly potentiated both LPS-induced lethality, as well as LPS-induced serum tumor necrosis factor alpha (TNF-α) activity. Although BALB/c-SCID mice were resistant to these LPS enhancement effects of TSST-1, BALB/c-SCID mice reconstituted with T cells were completely susceptible to the enhancement effect of TSST-1 on LPS-induced serum TNF-α. Mice pretreated with cyclosporine (Cs) or neutralizing antibodies against gamma interferon (IFN-γ) did not develop lethal LPS hypersensitivity when injected with TSST-1, and these agents reduced the enhancement effect of TSST-1 on LPS-induced serum TNF-α by 99 and 85%, respectively. Cs pretreatment also completely inhibited the known capacity of TSST-1 to amplify LPS-induced levels of IFN-γ in serum. In contrast, mice given Cs after a priming injection of TSST-1, but before LPS, still exhibited lethal hypersensitivity to LPS. Cs given after TSST-1 also did not inhibit enhancement of LPS-induced serum TNF-α by TSST-1 but inhibited the enhancement effect of TSST-1 on LPS-induced serum IFN-γ by 50%. These experiments support the theory that TSST-1-induced hypersensitivity to LPS is mediated primarily by IFN-γ derived from superantigen-activated T cells.
机译：毒性休克综合征毒素1（TSST-1）的超抗原功能通常被认为是其对人类或实验动物致死作用的重要决定因素。这项研究检查了超抗原性在致命的TSST-1诱导的对脂多糖（LPS）致敏的BALB / c小鼠模型中的作用。在此模型中，TSST-1大大增强了LPS诱导的致死性以及LPS诱导的血清肿瘤坏死因子α（TNF-α）的活性。尽管BALB / c-SCID小鼠对TSST-1的这些LPS增强作用有抵抗力，但用T细胞重构的BALB / c-SCID小鼠对TSST-1对LPS诱导的血清TNF-α的增强作用完全敏感。用环孢素（Cs）或抗γ干扰素（IFN-γ）的中和抗体预处理的小鼠注射TSST-1时不会产生致命的LPS超敏反应，并且这些药物降低了TSST-1对LPS诱导的血清TNF-α的增强作用。分别减少99％和85％。 Cs预处理还完全抑制了已知的TSST-1扩增LPS诱导的血清IFN-γ水平的能力。相反，在初次注射TSST-1之后但在LPS之前给予Cs的小鼠仍然表现出对LPS的致死性超敏反应。 TSST-1后给予的Cs也没有抑制TSST-1增强LPS诱导的血清TNF-α，但抑制了TSST-1对LPS诱导的血清IFN-γ的增强作用。这些实验支持以下理论：TSST-1诱导的对LPS的超敏性主要由源自超抗原激活的T细胞的IFN-γ介导。

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