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细菌诱导 I 型干扰素。

Induction of type I interferons by bacteria.

机构信息

Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.

出版信息

Cell Microbiol. 2010 Jul;12(7):881-90. doi: 10.1111/j.1462-5822.2010.01478.x. Epub 2010 May 6.

Abstract

Type I interferons (IFNs) are secreted cytokines that orchestrate diverse immune responses to infection. Although typically considered to be most important in the response to viruses, type I IFNs are also induced by most, if not all, bacterial pathogens. Although diverse mechanisms have been described, bacterial induction of type I IFNs occurs upon stimulation of two main pathways: (i) Toll-like receptor (TLR) recognition of bacterial molecules such as lipopolysaccharide (LPS); (ii) TLR-independent recognition of molecules delivered to the host cell cytosol. Cytosolic responses can be activated by two general mechanisms. First, viable bacteria can secrete stimulatory ligands into the cytosol via specialized bacterial secretion systems. Second, ligands can be released from bacteria that lyse or are degraded. The bacterial ligands that induce the cytosolic pathways remain uncertain in many cases, but appear to include various nucleic acids. In this review, we discuss recent advances in our understanding of how bacteria induce type I interferons and the roles type I IFNs play in host immunity.

摘要

I 型干扰素(IFNs)是分泌的细胞因子,可协调感染后的各种免疫反应。尽管通常认为 I 型 IFNs 对病毒的反应最重要,但它们也被大多数(如果不是全部)细菌病原体诱导。尽管已经描述了多种机制,但 I 型 IFNs 的细菌诱导是通过刺激两条主要途径发生的:(i)Toll 样受体(TLR)识别细菌分子,如脂多糖(LPS);(ii)TLR 非依赖性识别递送到宿主细胞质中的分子。细胞质反应可以通过两种一般机制激活。首先,存活的细菌可以通过专门的细菌分泌系统将刺激性配体分泌到细胞质中。其次,配体可以从裂解或降解的细菌中释放出来。在许多情况下,诱导细胞质途径的细菌配体仍不确定,但似乎包括各种核酸。在这篇综述中,我们讨论了我们对细菌如何诱导 I 型干扰素以及 I 型干扰素在宿主免疫中的作用的理解的最新进展。

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