Abstract
Alveolar echinococcosis (AE) is a deadly parasitic disease that requires lifelong treatment with albendazole. Development of host immunity is pivotal with regard to the clinical outcome of AE, but its influence on conventional albendazole treatment is unknown. Using T-cell deficient athymic nude mice, we demonstrated that functional immunity is required for albendazole to be efficacious against murine AE. These results call for attention given the increasing number of immunocompromised patients with AE.
Highlights
Alveolar Echinococcosis (AE) is a life-threatening disease caused by the metacestode stage of the fox tapeworm Echinococcus multilocularis
During E. multilocularis in fections in humans, a Th2-oriented immunity is basically associated with increased susceptibility to disease leading to chronic AE, while Th1 cell activation has been linked to protectivity, which may even yield aborted (“died-out”) forms of infection (Vuitton, 2003; Vuitton et al, 2006)
Increased CD4+CD25+ T regulatory cells (Tregs) were observed in peritoneal cells of mice intraperitoneally (i.p.) infected with E. multilocularis, and depletion of Foxp3+ Tregs led to an improved control of E. multilocularis infection (Wang et al, 2018)
Summary
Alveolar Echinococcosis (AE) is a life-threatening disease caused by the metacestode stage of the fox tapeworm Echinococcus multilocularis. During E. multilocularis in fections in humans, a Th2-oriented immunity is basically associated with increased susceptibility to disease leading to chronic AE, while Th1 cell activation has been linked to protectivity, which may even yield aborted (“died-out”) forms of infection (Vuitton, 2003; Vuitton et al, 2006). Human patients’ records suggest that the periparasitic immune response gradually increases throughout ABZ-treatment (Ricken et al, 2017), but confirmatory placebo-controlled studies are lacking.
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