Abstract
Human schistosomes combat the unique immune systems of two vastly different hosts during their indirect life cycles. In gastropod molluscs, they face a potent innate immune response composed of variable immune recognition molecules and highly phagocytic hemocytes. In humans, a wide variety of innate and adaptive immune processes exist in proximity to these parasites throughout their lifespan. To survive and thrive as the second most common parasitic disease in humans, schistosomes have evolved many techniques to avoid and combat these targeted host responses. Among these techniques are molecular mimicry of host antigens, the utilization of an immune resistant outer tegument, the secretion of several potent proteases, and targeted release of specific immunomodulatory factors affecting immune cell functions. This review seeks to describe these key immune evasion mechanisms, among others, which schistosomes use to survive in both of their hosts. After diving into foundational observational studies of the processes mediating the establishment of schistosome infections, more recent transcriptomic and proteomic studies revealing crucial components of the host/parasite molecular interface are discussed. In order to combat this debilitating and lethal disease, a comprehensive understanding of schistosome immune evasion strategies is necessary for the development of novel therapeutics and treatment plans, necessitating the discussion of the numerous ways in which these parasitic flatworms overcome the immune responses of both hosts.
Highlights
TO SCHISTOSOMES/IMMUNOSUPPRESSIONAll organisms must deal with threats in their environments to survive and thrive
Work demonstrated that mammalian effector cells such as neutrophils and eosinophils are capable of killing schistosomulae in vitro, especially in the presence of complement proteins and anti-schistosome immunoglobulins [63,64,65]
To counter the numerous challenges schistosomes face in their definitive hosts, these worms have developed several immune evasion mechanisms allowing for high infection loads and lifespans up to 37 years, indicating their capacity to survive and thrive despite the host immune response [71]
Summary
After leaving their snail intermediate host, cercaria move to the surface of the water column in the hopes of encountering a compatible mammalian host. In 2012, it was shown that W-1’s glycosylation patterns allow it to be internalized by DCs via binding to the mannose receptor, while ribonuclease activity results in lowered protein synthesis via the cleavage of host rRNA and mRNA [183] The significance of this molecule in driving the immune response surrounding schistosome eggs was recently demonstrated in the first ever published occurrence of CRISPR-mediated knockout of a S. mansoni gene, which resulted in a decrease in Th2 cytokine production from macrophage/T cell co cultures, while decreasing the volume of murine pulmonary granulomas [184]. These immune modulating and immune evading tactics allow for the egg to migrate through the host intestine/bladder, so that they may eventually be excreted in order to commence their life cycle anew
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