White A C, Robinson P, Kuhn R
Department of Medicine, Baylor College of Medicine, Houston, Tex, USA.
Chem Immunol. 1997;66:209-30.
Taenia parasites have developed elaborate mechanisms of interacting with their intermediate hosts. The oncospheres which invade the intermediate host are susceptible to antibody and complement. However, by the time the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode. The metacestodes have elaborate means of evading complement-mediated destruction, including paramyosin which inhibits C1q, taeniaestatin which inhibits both classical and alternate pathways, and sulfated polysaccharides which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. In fact, 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 poorly defined factors may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Since the symptoms of NCC are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily caused by injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of NCC, as well as in the evaluation of clinical trials, most of which were uncontrolled.
绦虫寄生虫已经形成了与中间宿主相互作用的复杂机制。侵入中间宿主的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抵抗力的绦虫蚴。绦虫蚴有多种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绦虫蚴。事实上，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，绦虫抑素和其他定义不明确的因素可能会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，我们推测该疾病主要由受损或即将死亡的寄生虫引起。这一假设在评估化疗在神经囊尾蚴病管理中的作用以及在评估临床试验（其中大多数是无对照的）方面提出了重要问题。
