HUMAN immune responses to schistosome infection have been characterized in detail^1–5. But there has been controversy⁶ over the relative importance of ecological factors (variation in exposure to infection) and immunological factors (acquired immunity) in determining the relationships between levels of infection and age typically found in areas where infection is endemic^7,8. Independent effects of exposure and age on the rates of reinfection with Schistosoma haematobium after chemotherapy have been demonstrated in the Gambia⁹ and Zimbabwe⁸. This age effect could be the result of acquired immunity to infection. Indeed, allowing for variation in exposure and age, low rates of reinfection in the Gambia are correlated with high amounts of specific IgE antibodies¹⁰―human IgE can kill S. mansoni schistosomulae in vitro¹¹. Further, animals can acquire immunologically mediated resistance to S. mansoni infection^12–14, although nonimmunological factors could also be involved¹⁵. Acquisition of this immunity seems to be related to the cumulative effects of repeated infection and provides only partial protection^12,13,16. These characteristics are consistent with immuno-epidemiological data for both S. mansoni and S. haematobium infections of humans^4,17. We have now analysed age–prevalence data for human infection with S. haematobium, and find patterns of variation that are indeed consistent with the epidemiological effects of acquired immunity predicted by mathematical models.