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I 型干扰素抑制 II 型干扰素引发的人体抗分枝杆菌反应。

Type I interferon suppresses type II interferon-triggered human anti-mycobacterial responses.

机构信息

Division of Dermatology, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, USA.

出版信息

Science. 2013 Mar 22;339(6126):1448-53. doi: 10.1126/science.1233665. Epub 2013 Feb 28.

DOI:10.1126/science.1233665
PMID:23449998
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3653587/
Abstract

Type I interferons (IFN-α and IFN-β) are important for protection against many viral infections, whereas type II interferon (IFN-γ) is essential for host defense against some bacterial and parasitic pathogens. Study of IFN responses in human leprosy revealed an inverse correlation between IFN-β and IFN-γ gene expression programs. IFN-γ and its downstream vitamin D-dependent antimicrobial genes were preferentially expressed in self-healing tuberculoid lesions and mediated antimicrobial activity against the pathogen Mycobacterium leprae in vitro. In contrast, IFN-β and its downstream genes, including interleukin-10 (IL-10), were induced in monocytes by M. leprae in vitro and preferentially expressed in disseminated and progressive lepromatous lesions. The IFN-γ-induced macrophage vitamin D-dependent antimicrobial peptide response was inhibited by IFN-β and by IL-10, suggesting that the differential production of IFNs contributes to protection versus pathogenesis in some human bacterial infections.

摘要

I 型干扰素(IFN-α 和 IFN-β)对于预防多种病毒感染很重要,而 II 型干扰素(IFN-γ)对于宿主抵抗某些细菌和寄生虫病原体的防御至关重要。对人类麻风病中的 IFN 反应的研究表明,IFN-β 和 IFN-γ 基因表达谱之间存在反比关系。IFN-γ 及其下游维生素 D 依赖性抗菌基因在自行愈合的结核样病变中优先表达,并在体外对病原体麻风分枝杆菌发挥抗菌活性。相比之下,IFN-β 及其下游基因,包括白细胞介素 10(IL-10),在体外由麻风分枝杆菌诱导单核细胞中表达,并在弥散性和进行性瘤型病变中优先表达。IFN-γ 诱导的巨噬细胞维生素 D 依赖性抗菌肽反应被 IFN-β 和 IL-10 抑制,这表明 IFN 的差异产生有助于某些人类细菌感染中的保护与发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/aa7f7792ee5b/nihms465501f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/63a25a173aeb/nihms465501f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/cf66b67be08b/nihms465501f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/77334b636c75/nihms465501f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/aa7f7792ee5b/nihms465501f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/63a25a173aeb/nihms465501f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/cf66b67be08b/nihms465501f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/77334b636c75/nihms465501f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b5/3653587/aa7f7792ee5b/nihms465501f4.jpg

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