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在M. tuberculosis感染期间中性粒细胞介导的免疫病理学中ATG5的独特作用

Jacqueline M Kimmey¹, Jeremy P Huynh¹, Leslie A Weiss¹

¹Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA.

|December 10, 2015

概括

自食不确定结核病的结果. 相反,ATG5蛋白质阻止了中性粒细胞引起的免疫病态,揭示了它在控制Mycobacterium结核病感染和天生的免疫力方面的独特作用.

科学领域:

免疫学
细胞生物学
微生物学

背景情况:

结核菌通过阻断巨细胞中的菌体-溶酶体融合来抑制宿主防御.
干扰素- (IFNγ) 激活巨细胞以清除M.结核病,但可能涉及自的机制尚不清楚.
之前的研究表明基于细胞培养的自作用对细菌复制有适度的影响.

研究的目的:

在体内基因研究与自相关的基因对M.结核病感染的抵抗性.
澄清M.结核病感染期间除了自外的ATG5的特定功能.
确定自能力与M.结核病感染结果之间的相关性.

主要方法:

在M.结核病感染的小鼠模型中对自相关基因的基因分析.
在具有向基因删除的小鼠中评估M.结核病的复制和宿主免疫病理.
评估不同类型的免疫细胞中的ATG5功能,包括巨细胞和中性粒细胞.

主要成果:

自能力与M.结核病感染结果没有相关性.
在预防中性粒细胞介导的免疫病理方面,ATG5扮演着关键的,独立于自的角色.
在对M.结核病感染敏感的小鼠中失去了ATG5,但没有膜巨细胞.

结论:

通过调节先天免疫反应和预防免疫病理,ATG5对M.结核有独特的保护功能.
在体内,自并不是抗M.结核病感染的主要驱动因素.
这些发现重新定义了ATG5在宿主防御中的作用,并强调了它在控制疾病进展和细菌复制方面的重要性.

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