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Syk/CARD9 偶联受体 Dectin-1 对于小鼠宿主抵抗结核分枝杆菌并不必需。

The Syk/CARD9-coupled receptor Dectin-1 is not required for host resistance to Mycobacterium tuberculosis in mice.

机构信息

Division of Immunology, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, South Africa.

出版信息

Microbes Infect. 2011 Feb;13(2):198-201. doi: 10.1016/j.micinf.2010.10.013. Epub 2010 Oct 27.

Abstract

There is interest in identifying the pattern recognition receptors involved in initiating protective or non-protective host responses to Mycobacterium tuberculosis (Mtb). Here we explored the role of the Syk/CARD9-coupled receptor, Dectin-1, using an aerosol model of Mtb infection in wild-type and Dectin-1 deficient mice. We observed a reduction in pulmonary bacilli burdens in the Dectin-1 deficient animals, but this did not correlate with significant changes in pulmonary pathology, cytokine levels or ability of these animals to survive the infection. Thus Dectin-1 makes a minor contribution to susceptibility to Mtb infections in mice.

摘要

人们对于鉴定与分枝杆菌(Mycobacterium tuberculosis,Mtb)引发保护或非保护宿主反应相关的模式识别受体很感兴趣。在此,我们利用分枝杆菌感染的气溶胶模型,在野生型和 Dectin-1 缺陷型小鼠中探索了 Syk/CARD9 偶联受体 Dectin-1 的作用。我们观察到 Dectin-1 缺陷型动物肺部细菌负荷减少,但这与肺部病理学、细胞因子水平或这些动物在感染中存活能力的显著变化无关。因此,Dectin-1 在小鼠对 Mtb 感染的易感性方面贡献较小。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/429e/3032049/6ce8e0cb4457/gr1.jpg

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