首页> 外文期刊>Cellular immunology >DosR antigen Rv1737c induces activation of macrophages dependent on the TLR2 pathway
【24h】

DosR antigen Rv1737c induces activation of macrophages dependent on the TLR2 pathway

机译:Dosr抗原RV1737C诱导巨噬细胞的激活取决于TLR2途径

获取原文
获取原文并翻译 | 示例
           

摘要

Latent Mycobacterium tuberculosis (Mtb) infection (LTBI) is the main clinical manifestation after Mtb exposure. During the latent phase, Mtb retards the attempts of eradication by the host immune system. The dormancy survival regulator (DosR) is held as essential for Mtb persistence. Rv1737c is predominantly expressed by the Mtb in latent infection. However, the role of Rv1737c in the immune evasion is still largely unknown. In this study, we have characterized the Rv1737c functions in the recruitment and activation of macrophages, which play a cardinal role in the innate and adaptive immunity. For the first time, we have revealed that Rv1737c induced the tolerogenic phenotype of macrophages by upregulating the expression of indoleamine 2,3-dioxygenase 1 (IDO1). Rv1737c-activated macrophages upregulated interleukin (IL)-4, IL-10, and Foxp3 T cells proliferation in vitro. Furthermore, the interaction of Rv1737c with macrophages was found to depend on the Toll-like receptor 2 (TLR2) pathway. It augmented nuclear factor kappa B (NF-kappa B) phosphorylation and co-stimulatory molecule expression. Thus, this study provides a crucial insight into a strategy adopted by Mtb to survive in the host by inducing tolerogenic macrophage expansion.
机译:结核分枝杆菌(MTB)感染(LTBI)是MTB暴露后的主要临床表现。在潜在阶段,MTB延迟了宿主免疫系统消除的尝试。休眠存活调节器(DOSR)对MTB持久性至关重要。 RV1737C主要由MTB在潜在感染中表达。然而,RV1737C在免疫逃避中的作用仍然很大程度上是未知的。在这项研究中,我们的特征在于募集和激活巨噬细胞的RV1737C功能,在先天和适应症中起着基本作用。我们首次透露,RV1737C通过上调吲哚胺2,3-二氧化酶1(IDO1)的表达来诱导巨噬细胞的耐受性表型。 RV1737℃激活的巨噬细胞上调的白细胞介素(IL)-4,IL-10和FoxP3 T细胞在体外增殖。此外,发现RV1737C与巨噬细胞的相互作用取决于Toll样受体2(TLR2)途径。它增强了核因子κB(NF-Kappa B)磷酸化和共刺激分子表达。因此,本研究通过诱导耐受性巨噬细胞扩张,对MTB采用的策略进行了重要的洞察力,以在宿主中存活。

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