Current Understanding of Immunity Against Schistosomiasis: Impact on Vaccine and Drug Development

Abstract

Schistosomiasis is a neglected tropical disease inflicting significant morbidity in humans worldwide. The disease is caused by infections with a parasitic trematode belonging to the genus Schistosoma. Over 250 million people are currently infected globally, with an estimated disability-adjusted life-years of 1.9 million attributed to the disease. Current understanding, based on several immunological studies using experimental and human models of schistosomiasis, reveals that complex immune mechanisms play off each other in the acquisition of immune resistance to infection/reinfection. Nevertheless, the precise characteristics of these responses, the specific antigens against which they are elicited, and how these responses are intricately regulated are still being investigated. What is apparent is that immunity to schistosome infections develops slowly and over a prolonged period of time, augmented by the death of adult worms occurring naturally or by praziquantel therapy. In this review, aspects of immunity to schistosomiasis, host-parasite interactions and their impact on schistosomiasis vaccine development are discussed.

Keywords: immunity; resistance to reinfection; schistosomiasis; schistosomiasis vaccine development.

Figure 1

Induction of host immune responses after infection with schistosomes. Following infection with schistosomes, the early immune response that develops is a T helper 1 (Th1)-dependent cellular response. As the worms mature into adults and the females start to lay eggs, there is an increased production of interleukin-10 (IL-10) by dendritic cells, and a Th2 response ensues. In addition, B cells produce IL-10 in response to antigens derived from eggs and adult worms. Populations of regulatory T cells and alternatively activated macrophages also develop. Image created with BioRender (app.biorender.com)