Immune expulsion of helminth parasites is driven by two key pathways mediated by soluble cytokines ligating to the IL-4 and IL-25 receptors acting on innate effector cells throughout the course of infection.
In a Ugandan birth cohort, early childhood infection-exposure, notably to malaria, helminths, and diarrhoea, is associated with lower prevalence of atopy and allergy-related diseases in later childhood.
Macrophage dynamics are fundamentally different between two commonly used inbred mouse strains and differences in local resident cell expansion versus monocyte recruitment determine the outcome of tissue nematode infection.
Parasitic helminths infect over a billion humans and use unusual anaerobic metabolism that needs a rare electron carrier, Rhodoquinone (RQ), whose synthesis requires the kynurenine pathway of tryptophan degradation.
A genome scale model of Brugia malayi metabolism illustrates a dynamic reliance on energy production pathways across its life cycle and identifies new drugs with experimentally supported anti-parasitic properties.