【摘要】 囊型棘球蚴病(Cystic echinococcosis, CE)(又称囊型包虫病)是一种全球性人畜共患病，是由动物源性寄生虫细粒棘球绦虫感染引起的，狗是其最适宜的终末宿主，也是该病的主要传染源，羊为主要中间宿主，牛、马、猪、骆驼等也能够感染此寄生虫，并成为传染源。人类感染者主要经过消化道误食虫卵或者与已经感染的动物密切接触而被感染，细粒棘球绦虫的虫体能够寄生于人体肝脏及全身各处，其慢性感染过程涉及宿主与寄生虫间复杂的免疫互作。细胞自噬(Autophagy)是真核生物中高度保守的细胞降解和循环过程，参与饥饿、细胞分化、细胞死亡等多种生理过程和疾病过程的调节。近年研究发现，细胞自噬作为宿主细胞内稳态的核心调控机制，在寄生虫的免疫逃逸、包囊存活及宿主组织损伤中发挥了双重作用。本文系统综述了自噬相关信号通路(如mTOR、AMPK、PI3K-AKT)、细胞自噬关键分子(如LC3、Beclin-1、p62)在囊型棘球蚴病的病理进程中的机制作用，探讨寄生虫来源的分子(如抗原B、EgTeg)对宿主自噬的调控机制，期望能够为靶向自噬的潜在治疗策略以及相关药物研发提供重要的理论依据。更多还原

【Abstract】 Cystic echinococcosis(CE) also known as cystic hydatid disease,is a zoonotic disease with global prevalence caused by infection with the animal-derived parasite Echinococcus granulosus. Dogs are the most appropriate definitive hosts and primary sources of transmission for this disease, whereas sheep serve as the principal intermediate hosts. Other livestock, such as cattle, horses, pigs, and camels, can also be infected by this parasite and serve as transmission reservoirs. Human infection mainly occurs through accidental ingestion of parasite eggs via the digestive tract or close contact with infected animals. The larvae of E. granulosus can parasitize various tissues throughout the human body, particularly the liver, with its chronic infection process involving intricate immune interactions between the host and parasite. Autophagy, a highly conserved cellular degradation and recycling mechanism in eukaryotes, plays a crucial role in regulating a wide range of physiological and pathological processes such as nutrient deprivation, cellular differentiation, and programmed cell death. Recent studies have demonstrated that autophagy, serving as a fundamental regulatory mechanism for intracellular homeostasis in host cells, exerts dual effects on parasite immune evasion, cyst survival, and host tissue damage. This review systematically examines the mechanistic involvement of autophagy-related signaling pathways(such as mTOR,AMPK,PI3K-AKT) and key autophagy molecules(such as LC3,Beclin-1,p62) in the pathological process of cystic echinococcosis, and it further explores the regulatory mechanism of parasite-derived molecules(such as Antigen B and EgTeg) on host autophagy, aiming to provide critical theoretical foundations for developing autophagy-targeted therapeutic strategies and related pharmacological interventions.更多还原