Infections with parasitic trematodes of the genus Schistosoma affect 200 million people worldwide, primarily in developing countries. Studies involving S. mansoni have suggested that successful completion of parasite development and migration within the mammalian host is dependent on the receipt of appropriate host-derived signals by the parasite and on transmission of signals between male and female parasites. A molecular understanding of the signals and receptors involved in these interactions may reveal new opportunities to disrupt the parasite life cycle for therapeutic or prophylactic purposes. We have now found that normal development of S. mansoni in the murine host is dependent on adaptive immune responses mounted by the host during prepatency.
The aims of this proposal are to (i) identify the precise immune cells and factors responsible for promoting parasite development, and (ii) identify parasite molecules involved in mediating phenotypic plasticity to host factors. The ultimate goal of this work is to identify novel mechanisms for disrupting the parasite life cycle for therapeutic and prophylactic purposes
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