Suppr超能文献

致病性肠炎沙门氏菌对T细胞免疫的逃避

T cell immunity evasion by virulent Salmonella enterica.

作者信息

Bueno Susan M, González Pablo A, Schwebach J Reid, Kalergis Alexis M

机构信息

Millennium Nucleus on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Chile.

出版信息

Immunol Lett. 2007 Jul 31;111(1):14-20. doi: 10.1016/j.imlet.2007.05.003. Epub 2007 Jun 6.

Abstract

Salmonella enterica are Gram-negative bacteria that cause systemic disease in their specific hosts. One of the recently appreciated features of Salmonella pathogenicity is the capacity of the bacteria to impair host adaptive immunity by interfering with DC function and T cell activation. It is likely that this feature of virulent Salmonella is needed to promote systemic dissemination in the host. Recent studies have suggested explanations for some of the molecular mechanisms developed by virulent Salmonella to impair DC and T cell function. Several of these mechanisms require the expression of virulence genes encoded within Salmonella pathogenicity islands. Targeted deletion of these genes diminishes Salmonella pathogenicity and leads to efficient activation of T cells by Salmonella-infected DCs. In this review, recent data that support the subversion of DC function by Salmonella as a means to evade host adaptive immunity and cause systemic infection are discussed. These new findings suggest a new pathogenesis model with DCs as key targets for Salmonella virulence factors.

摘要

肠炎沙门氏菌是革兰氏阴性菌,可在其特定宿主中引发全身性疾病。沙门氏菌致病性的一个最近才被认识到的特征是,该细菌能够通过干扰树突状细胞(DC)功能和T细胞活化来损害宿主的适应性免疫。致病性沙门氏菌的这一特征可能是促进其在宿主体内全身性传播所必需的。最近的研究对致病性沙门氏菌所形成的一些损害DC和T细胞功能的分子机制提出了解释。其中一些机制需要沙门氏菌致病岛中编码的毒力基因的表达。靶向删除这些基因会降低沙门氏菌的致病性,并导致受沙门氏菌感染的DC有效激活T细胞。在这篇综述中,讨论了支持沙门氏菌颠覆DC功能作为逃避宿主适应性免疫并导致全身性感染手段的最新数据。这些新发现提示了一种新的发病机制模型,即以DC作为沙门氏菌毒力因子的关键靶点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验