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.

HpBARI is a protein secreted by a parasitic helminth, which binds to and blocks the IL-33 receptor, suppressing IL-33-dependent type 2 immune responses.

The HpARI family members can either suppress or amplify responses to IL-33, and also differ in their half-life in vivo due to binding to the extracellular matrix constituent, heparan sulphate.

A systematic optimization of intestinal digestion protocols allows for the isolation and high-dimensional flow cytometric analysis of intestinal immune cells during murine helminth infection.

The small macrophage-secreted protein RELMα is a sex-specific protein that protects against diet-induced obesity through regulating the macrophage–eosinophil innate immune axis in the adipose tissue.

The absence of helminth parasites in developed countries may be exacerbating pathological, age-associated inflammation, known as inflammaging, suggesting that helminth therapies could provide protection against age-related disease.

The expression of DECTIN-2 family C-type lectin receptors on macrophages and monocytes is inhibited by the Th2 cytokine IL-4, which suggests a mechanism for inhibition of Th17 responses to MINCLE-dependent vaccination responses by underlying helminth infection.

Th2 cell heterogeneity was revealed by combined transcriptome and T-cell receptor sequencing of single Th2 cells from lung and lymph node of helminth-infected mice and led to identification of a helminth-specific T-cell receptor.

Helminth infected hosts are an important cause of variation in the level, frequency and duration of Bordetella bronchiseptica shedding and dynamics of infection.