Schistosomiasis protective immunity

In the context of schistosomiasis, where parasites do not multiply in the mammalian host, protective immunity is primarily measured as a reduction in the adult worm burden of vaccinated animals relative to controls. Conventionally, this has been assessed by a terminal procedure involving perfusion of the portal... 

James, S.L. (1986) Activated macrophages as effector cells of protective immunity to schistosomiasis. Immunologic Research 5, 1 39-148. 

James, S.L. and Pearce, E.J. (1 988) The influence of adjuvant on induction of protective immunity by a nonliving vaccine against schistosomiasis. The Journal of Immunology 1 40, 2753-2759. 

In an excellent review of the immunopathogenesis of schistosomiasis, Warren (W3) reported that the egg of the schistosome parasite was the prime factor responsible for the hepatosplenomegaly in the mouse furthermore, that neonatal thymectomy and antilymphocyte serum had marked immunosuppression on the granuloma formation around schistosome eggs injected into the lungs of mice, implying that cell-mediated immunity must play some role in the protection of the host against schistosome infection. 

This report will detail current knowledge of the role of IgE in mediating immunity to helminth parasites. Because IgE responses to helminth infections differ based on chronicity of infection, the life cycle of the parasite, and the parasite s location within the host, it is difficult to apply data from one parasite to those of another, particularly in theorizing about the potential effects of anti-IgE therapy. The report will focus, in particular, on schistosomiasis and strongyloidiasis, for which most observational and experimental data have been accumulated to support a protective role for IgE. The latter infection is of particular relevance because of its unusual capacity to replicate within the human host, so-called auto-infection. Although most of the discussion will rely on data from human studies, much of this information is incomplete, and, where appropriate, observations from experimental animal models will be included. 

In many endemic areas, first infection with schistosomes occurs at a young age (approximately 4 years) (4). Because of early exposure and infection, older children and adults can be considered to have chronic infections however, it should be remembered that although younger children may have hyperreactive immune responses to schistosome antigens (26), these undergo profound changes through later childhood and adulthood (27,28). Numerous observational field studies of human schistosomiasis have indicated a protective role for IgE. 

A principal tenet of the IgE-protection hypothesis in schistosomiasis is that immunity is slowly acquired (26,28), is dependent on the period of exposure (e.g., age-dependent in endemic areas), and may only be partial (42). These factors have been proposed to explain the characteristic age-intensity curves in which peak infection levels occur in late childhood. The decline in intensity in early adult hood that cannot be explained suffleiently by changes in exposure is taken as evidence of age-acquired immunity (26,28). Recent immunological studies of communities with recently acquired exposure, however, demonstrate age-intensity profiles similar to those seen in endemic areas (8,28,43). Such observations argue for the importance of other age-dependent resistance mechanisms, including... 

---