结核性肉芽肿的代谢免疫调控机制研究进展

Research progress on immunometabolism regulatory mechanisms of tuberculous granuloma

摘要:

结核病仍然严重威胁人类健康。结核性肉芽肿是结核病的典型病理特征，也是结核分枝杆菌Mtb逃避宿主免疫杀伤实现长期存活及潜伏感染的“避难所”。结核分枝杆菌还利用肉芽肿促进其在体内扩散和传播，导致疾病迁延不愈，难以根除。肉芽肿环境中的代谢级联反应和免疫细胞产生的相关代谢物在疾病进展和诱导抗结核保护性免疫中发挥关键作用。 而 Mtb可以通过自身毒力因子，靶向宿主关键代谢通路抵抗免疫防御，实现长期存活并伺机增殖促进肉芽肿进展。本文对结核性肉芽肿中 Mtb与宿主相互作用的关键代谢免疫通路及其调控机制展开论述，为后续靶向肉芽肿发病进程开发新的结核病防治策略提供参考。

Abstract:

Tuberculosis (TB) remains a significant threat to human health. Tuberculous granuloma is a typical pathological feature of TB and also a "refuge" for Mycobacterium tuberculosis (Mtb) to escape host immune defense and achieve long-term survival and latent infection. Mtb exploits these granulomas to spread and propagate within the body, leading to persistent infections that are difficult to eradicate. The metabolic cascade reactions and metabolites produced by immune cells in the granuloma environment are crucial for disease progression and the induction of protective anti-tuberculosis immunity. Mtb can use its virulence factors to target key host metabolic pathways, resist immune defenses, achieve long-term survival, and promote granuloma progression. This paper discusses the key immunometabolism pathways and the regulation mechanism of Mtbhost interaction in granuloma. It provides insights for developing new tuberculosis prevention and treatment strategies targeting granuloma pathogenesis.