• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Gamma Interferon Modulates CD95 (Fas) and CD95 Ligand (Fas-L) Expression and Nitric Oxide-Induced Apoptosis during the Acute Phase ofTrypanosoma cruzi Infection: a Possible Role in Immune Response Control
【24h】

Gamma Interferon Modulates CD95 (Fas) and CD95 Ligand (Fas-L) Expression and Nitric Oxide-Induced Apoptosis during the Acute Phase ofTrypanosoma cruzi Infection: a Possible Role in Immune Response Control

机译：γ干扰素调节克氏锥虫感染急性期期间的CD95（Fas）和CD95配体（Fas-L）表达和一氧化氮诱导的细胞凋亡：在免疫反应控制中的可能作用。

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

摘要

We have previously shown that splenocytes from mice acutely infected with Trypanosoma cruzi exhibit high levels of nitric oxide (NO)-mediated apoptosis. In the present study, we used the gamma interferon (IFN-γ)-knockout (IFN-γ?/?) mice to investigate the role of IFN-γ in modulating apoptosis induction and host protection during T. cruzi infection in mice. IFN-γ?/? mice were highly susceptible to infection and exhibited significant reduction of NO production and apoptosis levels in splenocytes but normal lymphoproliferative response compared to the infected wild-type (WT) mice. Furthermore, IFN-γ modulates an enhancement of Fas and Fas-L expression after infection, since the infected IFN-γ?/? mice showed significantly lower levels of Fas and Fas-L expression. The addition of recombinant murine IFN-γ to spleen cells cultures from infected IFN-γ?/?mice increased apoptosis levels, Fas expression, and NO production. In the presence of IFN-γ and absence of NO, although Fas expression was maintained, apoptosis levels were significantly reduced but still higher than those found in splenocytes from uninfected mice, suggesting that Fas–Fas-L interaction could also play a role in apoptosis induction in T. cruzi-infected mice. Moreover, in vivo, the treatment of infected WT mice with the inducible nitric oxide synthase inhibitor aminoguanidine also led to decreased NO and apoptosis levels but not Fas expression, suggesting that IFN-γ modulates apoptosis induction by two independent and distinct mechanisms: induction of NO production and of Fas and Fas-L expression. We suggest that besides being of crucial importance in mediating resistance to experimentalT. cruzi infection, IFN-γ could participate in the immune response control through apoptosis modulation.
机译：先前我们已经证明，急性感染克氏锥虫的小鼠的脾细胞表现出高水平的一氧化氮（NO）介导的细胞凋亡。在本研究中，我们使用了γ-干扰素（IFN-γ）-敲除（IFN-γ？/？）小鼠来研究IFN-γ在< em> T。小鼠中的cruzi 感染。与感染的野生型（WT）小鼠相比，IFN-γα/β小鼠对感染高度敏感，并表现出脾细胞中NO产生和凋亡水平的显着降低，但淋巴细胞增生反应正常。此外，IFN-γ调节感染后Fas和Fas-L表达的增强，因为被感染的IFN-γα/β小鼠表现出明显降低的Fas和Fas-L表达水平。在感染的IFN-γ？/？小鼠的脾细胞培养物中加入重组鼠IFN-γ可增加细胞凋亡水平，Fas表达和NO的产生。在存在IFN-γ和不存在NO的情况下，尽管Fas表达得以维持，但凋亡水平显着降低，但仍高于未感染小鼠脾细胞中发现的水平，这表明Fas-Fas-L相互作用也可能在凋亡中起作用在 T中的归纳。克鲁兹感染的小鼠。此外，在体内，用可诱导的一氧化氮合酶抑制剂氨基胍治疗感染的WT小鼠也导致NO和凋亡水平降低，但不导致Fas表达降低，这表明IFN-γ通过两种独立且不同的机制调节凋亡诱导： Fas和Fas-L表达的产生和表达。我们建议除了在介导对实验性T的抵抗中至关重要。感染克鲁斯病后，IFN-γ可通过凋亡调节参与免疫应答的控制。

著录项

相似文献

  • 外文文献
  • 中文文献
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