White A C, Tato P, Molinari J L
Department of Medicine, Baylor College of Medicine, Houston, TX 77030.
Infect Agents Dis. 1992 Aug;1(4):185-93.
Human neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue cyst) of Taenia solium. Cysticercosis is being increasingly recognized as a cause of neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading complement-mediated destruction, including paramyosin, which inhibits C1q; taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting factor D and C3 esterase); and sulfated polysaccharides, which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via Fc receptors, and used as a source of protein. Finally, taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.
人类神经囊尾蚴病是由猪带绦虫的囊尾蚴（组织囊肿）形式侵袭中枢神经系统所致。囊尾蚴病越来越被认为是发展中国家居民和移民出现神经症状的一个原因。带科寄生虫已形成了复杂的机制以在其中间宿主组织中存活。侵入性幼虫，即六钩蚴，易受抗体和补体的影响。然而，当宿主产生抗体反应时，寄生虫已开始转变为更具抗性的囊尾蚴形式。囊尾蚴也有逃避补体介导破坏的方式，包括抑制C1q的副肌球蛋白；抑制经典途径和替代途径（可能是通过抑制因子D和C3酯酶）的绦虫抑素；以及使补体远离寄生虫激活的硫酸化多糖。同样，抗体似乎也无法杀死成熟的囊尾蚴。寄生虫甚至可能刺激宿主产生抗体，这些抗体可通过Fc受体结合，并用作蛋白质来源。最后，绦虫抑素和其他寄生虫分子可能干扰淋巴细胞增殖和巨噬细胞功能，从而使细胞免疫反应瘫痪。由于神经囊尾蚴病的症状通常与活跃的炎症反应相关，我们推测该病主要是受损或即将死亡的寄生虫所致。这一推测在评估化疗在神经囊尾蚴病治疗中的作用以及在评估临床试验（其中大多数未设对照）时引发了重要问题。
