Murine Schistosomiasis

Control of schistosomiasis using conventional means is lifelong and expensive. A relatively inexpensive alternative would be a vaccine that either prevents or reduces infection or significantly reduces the occurrence of severe disease. Therefore, much of the current immunological work on schistosomiasis is focused on understanding the mechanisms of vaccine-induced immunity and the pathogenesis of granuloma formation so that defined and highly effective anti-infection and/or antipathology vaccines might be developed. Schistosomiasis is caused by three major species of helminth parasites, Schistosoma mansoni, Schistosoma haematobium, and Schistosoma japonicum. Additionally, monoclonal antibody (MAb) anti-interleukin 4 (IL-4) treatment of infected mice tends to reduce granuloma size and fibrosis, although the same outcome is not always observed when different strains of IL-4-deficient mice are studied. Importantly, while IL-4 and IL-13 are both required for maximal granuloma formation, IL-13 is the primary mediator of hepatic fibrosis. The overall relevance of the Th1-associated immunopathology reported in some studies of murine schistosomiasis remains unclear, since there is no published evidence of hepatocellular toxicity or cytokine-induced shock in humans infected with S. mansoni. In many parasitic infections, including schistosomiasis, disease is not always induced by the parasite but may instead be a direct consequence of the host immune response to the parasite. While characterization and development of defined anti-infection vaccines remain a high priority for schistosomiasis vaccine development, studies aimed at better understanding the pathogenesis of granuloma formation also remain an important area of future research.