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BackgroundCysticercosis is a severe foodborne zoonotic parasitosis infected by the metacestode larvae of Taenia solium. However, its invasion mechanism is still not clear, which might provide the important evidence for treatment or vaccine. It was reported the annexin involved in the physiological and pathological functions of Cysticercus cellulosae. However, the regulatory mechanisms and roles of annexin B1 and annexin B2 in the invasion and immune escape of Cysticercus cellulosae have not been fully explored.MethodsThe annexin was acquired by cloning in prokaryotic expression vector, expressed in Escherichia coli, and purified by affinity chromatography. Its expression was determined by immunohistochemistry. The anticoagulant function and its underlying mechanism was verified by the determination of activated partial thromboplastin time, prothrombin time and phospholipid binding activity. The membrane repair function was verified by cell culture, transfection, and laser confocal technology.ResultsImmunohistochemistry results showed the B1 and B2 were mainly expressed on the body surface and the surface of digestive glands of Cysticercus cellulosae. The Blood coagulation results illustrated the B1 and B2 can prolong the time of both exogenous and endogenous coagulation pathways, with B2 having a more significant effect. They tend to bind to phosphatidylserine, possibly interfering with coagulation complex formation and inhibiting the coagulation pathway, and may assist in the worm’s penetration through blood vessels and migration to parasitic sites. The plasma membrane repair test revealed the cells transfected with B1 and B2 genes have a significantly shorter plasma membrane repair time than the control group, suggesting that these proteins may be involved in repairing the worm’s body surface to resist the immune system’s attack when the host immune system attacks.ConclusionsThe Annexin B1 and Annexin B2 of Cysticercus cellulosae possess anticoagulant properties and can assist in membrane repair. Given these functions, it is speculated that they play a crucial role in immune evasion and invasion. However, further experiments are required to provide direct evidence to further validate these speculations.背景：囊尾蚴病（Cysticercosis）是由猪带绦虫（Taenia solium）的囊尾蚴幼虫感染引发的严重食源性人兽共患寄生虫病。然而其入侵机制至今尚未阐明，而该机制可为该病的治疗或疫苗研发提供关键依据。已有研究表明，膜联蛋白（annexin）参与猪囊尾蚴（Cysticercus cellulosae）的生理与病理过程，但膜联蛋白B1与膜联蛋白B2在猪囊尾蚴入侵及免疫逃逸中的调控机制与作用尚未得到充分探究。 方法：本研究通过原核表达载体克隆获取膜联蛋白基因，在大肠杆菌（Escherichia coli）中进行表达，并借助亲和层析技术完成纯化；采用免疫组织化学法检测其表达定位；通过活化部分凝血活酶时间（activated partial thromboplastin time）、凝血酶原时间（prothrombin time）检测及磷脂结合活性实验，验证其抗凝功能及其潜在作用机制；通过细胞培养、基因转染及激光共聚焦扫描显微镜技术（laser confocal technology）验证其膜修复功能。 结果：免疫组织化学结果显示，膜联蛋白B1与B2主要表达于猪囊尾蚴的体壁表面及消化腺表面。凝血功能实验表明，二者均可延长外源性与内源性凝血通路的活化时间，其中膜联蛋白B2的作用更为显著。二者倾向于结合磷脂酰丝氨酸（phosphatidylserine），推测其可通过干扰凝血复合物形成、抑制凝血通路，协助虫体穿透血管并迁移至寄生部位。质膜修复实验显示，转染B1与B2基因的细胞，其质膜修复时间显著短于对照组，提示这两种蛋白可参与修复虫体表面，以抵抗宿主免疫系统的攻击。 结论：猪囊尾蚴的膜联蛋白B1与膜联蛋白B2具备抗凝特性，并可辅助完成膜修复。基于上述功能，推测二者在免疫逃逸与入侵过程中发挥关键作用，但仍需开展进一步实验以提供直接证据，验证上述推测。