| pubmed-article:9103671 | pubmed:abstractText | 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. | lld:pubmed |
