Helminth infections modulate the immune system of their hosts. They induce a Th2 immune response that is characterized by eosinophilia, elevated IgE levels, and production of type 2 cytokines such as IL-4, IL-5, and IL-13. Over time, however, chronic helminth infections induce immunoregulatory networks through regulatory T cells, alternatively activated macrophages, and inhibitory cytokines like IL-10 and TGFβ.
While helminth-induced immunoregulation enhances parasite survival in the host, it also impacts the immune response to bystander antigens. Until recently, most people had lifelong helminth infections and findings of helminths in mummies, suggest that it is likely that the human immune system evolved in the presence of chronic helminth infections. The loss of helminth infections and the resulting unbalanced immune system is one possible explanation for the recent increase in allergies and autoimmune diseases in industrialized countries. This hypthesis is supported by several human and experimental animal studies, which showed that helminth infections ameliorate or prevent the onset of autoimmune diseases and allergies.
The focus of my group is to investigate the helminth-induced immunomodulation in the host. In particular, my group is interested in the anti-inflammatory potential of helminth infections in the context of a systemic inflammatory immune response (sepsis) and the mechanisms by which helminth infections prevent the onset of autoimmune diseases and ameliorate diet-induced glucose intolerance. Infections of mice with the rodent filarial nematode Litomosoides sigmodontis are used to investigate these topics with the ultimate goal to develop new helminth-derived therapeutic regiments for sepsis and autoimmune diseases.
In addition, we are working in close collaboration with industry partners, the Drugs for Neglected Disease Initiative (DNDi) and the Bill & Melinda Gates Foundation to identify macrofilaricidal drugs which are required to eliminate onchocerciasis and lymphatic filariasis.