Purpose of review: The mechanisms responsible for the Th2-mediated immune response to enteric nematode parasites are of interest for several reasons. First, intestinal parasites continue to be a major worldwide health issue. Second, the low incidence of parasite infection in industrial nations is cited as a factor in the increased prevalence of proinflammatory-based pathologies. Third, a seemingly paradoxical protection against Th2-mediated allergic reactions is afforded by helminth infection. This review focuses on studies that use enteral parasitic infections as a tool to investigate the functional consequences of upregulation of Th2-mediated immunity and that manipulate host-parasite interactions in an effort to identify mechanisms that can be exploited as potential therapeutic targets.
Recent findings: Enteric helminth infection improved indices of inflammatory bowel disease in humans and murine models and diminished the allergy-induced changes in pulmonary function. There are emerging or enlarged roles for interleukin-10, interleukin-18, interleukin-9, chemokines, activation of nuclear factor-kappabeta, and factors that alter host resistance in the development of host immunity, and for interleukin-13Ralpha2 receptor in downregulating Th2 responses. As part of the growing appreciation for the contribution of nonimmune cells to parasite-induced changes in intestinal function, studies show that Th2 cytokines exert Stat6-dependent effects that promote worm expulsion.
Summary: Further insight into the nature of host-parasite interactions, identification of the pathways and critical mediators that contribute to host resistance, identification of the factors that modulate susceptibility to infection, and the impact of enteric parasites on intestinal function hold much promise for development of novel therapeutic interventions.