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在Mycobacterium tuberculosis感染期间NRF2抑制膜巨细胞MHC II表达

Linh K Pham^1,2, Maritza M Cervantes¹, Pamelia N Lim^1,3

¹Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, Amherst, MA, USA.

bioRxiv : the preprint server for biology

|August 20, 2025

概括

虽然NRF2增强了Mycobacterium结核病感染期间的细胞保护,但却意外地阻碍了宿主免疫力. 它抑制了巨细胞中的MHC II表达,损害了CD4+T细胞激活和关键的先天适应性免疫交叉.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
微生物学微生物学

背景情况:

结核菌菌 (Mtb) 感染触发了膜巨细胞 (AMs) 中NRF2调节的保护性反应.
这种NRF2活性阻碍AM激活和MHC II表达,这对CD4+T细胞激活和宿主免疫至关重要.

研究的目的:

调查NRF2调节MHC II途径和在Mtb感染期间AMs中的抗原呈现的假设.
阐明NRF2对MHC II表达和T细胞激活在Mtb.的背景下对NRF2的影响.

主要方法:

在体外和体内研究涉及MTB感染在AMs.
对MHC I和MHC II表达的分析.
对Ciita和H2-Ab1.1的基因表达分析.
评估ESAT6特异性的CD4+T细胞激活.

主要成果:

在Mtb感染期间,NRF2特别抑制MHC II表达,但不是MHC I,在AMs中.
NRF2在AM中抑制Ciita和H2-Ab1基因表达,这种效应在先天性刺激和IFNγ暴露后持续存在.
受Mtb感染的AM体中NRF2表达减少了它们激活ESAT6特异性CD4+T细胞的能力.

结论:

在Mtb感染期间,NRF2介导的AM中MHC II的抑制会损害先天适应性免疫交叉.
这种NRF2功能限制了CD4+T细胞的激活,可能会损害宿主免疫力.
虽然NRF2提供细胞保护,但其在抑制MHC II中的作用在宿主防御结核病方面具有关键的脆弱性.

关键词:

CD4+ T 细胞是 CD4+ T 细胞.结核病菌菌菌的结核病菌的结核病菌.这就是NRF2的NRF2.膜细胞巨细胞抗原呈现的呈现方式.这是先天的免疫力.

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