Normal and T-cell deprived mice have been compared in their response to infection with Schistosoma bovis. The deprived mice survived longer than comparably infected, immunologically intact controls, despite an increased longevity of the adult S. bovis worms in the former animals giving rise to higher tissue egg densities. The reduced pathology in deprived mice was due to inhibition of T-cell dependent granuloma formation around tissue-bound schistosome eggs, with concomitantly decreased tissue disruption as evidenced by smaller spleens and lower circulating transaminase concentrations. These observations on S. bovis contrast with the greater morbidity and earlier mortality induced by S. mansoni in T-cell deprived mice, the latter due to an hepatotoxic potential of S. mansoni eggs that is expressed in the absence of the host immune response. The absence of hepatocyte damage around S. bovis eggs in deprived mice indicates that this schistosome lacks such a toxin, and this could explain why during S. bovis infection synthesis of the two acute-phase proteins, complement C3 and serum amyloid P-component (SAP) here seemed less T-dependent than has previously been found during S. mansoni infection of mice. In a time-course experiment the hypergammaglobulinaemia induced by S. bovis, and the specific IgG antibody response against egg antigens were significantly T-cell dependent during the early stages of patency. Similarly, in most experiments assayed once between 9 and 11 weeks after S. bovis infection, deprived mice had significantly reduced hypergammaglobulinaemias, and reduced specific IgM and IgG antibody responses against both worm and egg antigens.