...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Modulation of Murine Lyme Borreliosis by Interruption of the B7/CD28 T-Cell Costimulatory Pathway
【24h】

Modulation of Murine Lyme Borreliosis by Interruption of the B7/CD28 T-Cell Costimulatory Pathway

机译：通过中断B7 / CD28 T细胞共刺激途径对小鼠莱姆病的调制。

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

摘要

Recent studies have implicated cytokines associated with Th2 cells in the genetic resistance to murine Lyme borreliosis. Because the B7/CD28 costimulatory pathway has been shown to influence the differentiation of Th-cell subsets, we investigated the contribution of the B7 molecules CD80 and CD86 to the Th2 cytokine profile and development of arthritis in BALB/c mice infected with Borrelia burgdorferi. Effective blockade of CD86/CD28 interaction was demonstrated by elimination of interleukin 4 (IL-4) and upregulation of gamma interferon (IFN-γ) responses by B. burgdorferi-specific T cells and by reduction of B. burgdorferi-specific immunoglobulin G. Despite the shift toward a Th1 cytokine pattern, which others have associated with disease susceptibility, the severity of arthritis was unchanged. Moreover, combined CD80/CD86 blockade by using anti-CD80 and anti-CD86 monoclonal antibodies or CTLA-4Ig enhanced IFN-γ production over that seen with CD86 blockade alone, yet augmentation of this Th1-associated cytokine did not enhance disease. These results demonstrate that IL-4 production by T cells in B. burgdorferi-infected BALB/c mice is dependent upon CD86/CD28 interaction and that this cytokine does not contribute significantly to host resistance to the development of arthritis. In addition, combined CD80/CD86 blockade resulted in preferential expansion of IFN-γ-producing T cells in B. burgdorferi infection, suggesting that costimulatory pathways other than B7/CD28 may contribute to T-cell activation during continuous antigen stimulation. These studies may provide insight into the role of the B7/CD28 pathway in other infectious and autoimmune diseases in which deviation of Th cell immune responses occurs and antigen is persistently present.
机译：最近的研究表明，与Th2细胞相关的细胞因子与鼠类莱姆病的遗传抗性有关。由于已显示B7 / CD28共刺激途径影响Th细胞亚群的分化，因此我们研究了感染了的BALB / c小鼠中B7分子CD80和CD86对Th2细胞因子谱和关节炎发展的贡献。伯氏疏螺旋体。通过消除白介素4（IL-4）和 B上调γ干扰素（IFN-γ）反应，证明了对CD86 / CD28相互作用的有效阻断。 burgdorferi 特异的T细胞和 B的还原。 burgdorferi特异性免疫球蛋白G。尽管其他疾病与疾病易感性相关，Th1细胞因子也发生了变化，但关节炎的严重程度没有改变。此外，与单独使用CD86阻滞相比，使用抗CD80和抗CD86单克隆抗体或CTLA-4Ig联合进行CD80 / CD86阻滞增强了IFN-γ的产生，但是与Th1相关的细胞因子的增强并未增强疾病。这些结果证明在 B中由T细胞产生IL-4。感染了伯氏疏螺旋体的BALB / c小鼠依赖于CD86 / CD28相互作用，并且这种细胞因子对宿主对关节炎发展的抗性没有明显贡献。另外，结合的CD80 / CD86阻断导致 B中产生IFN-γ的T细胞优先扩增。 burgdorferi感染，表明在持续的抗原刺激过程中，除B7 / CD28以外的共刺激途径可能有助于T细胞活化。这些研究可以提供对B7 / CD28途径在其他感染性和自身免疫性疾病中的作用的洞察力，在这些疾病中，Th细胞免疫反应发生偏差，并且抗原持续存在。

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