Abnormalities of immunosuppression in patients with hepatosplenic schistosomiasis mansoni.

The basis for development of hepatosplenic disease and attendant morbidity in only a minority of S. mansoni-infected individuals is uncertain but may relate to defective modulation of immunopathology. We explored the possibility that schistosomiasis mansoni with hepatosplenomegaly is characterized by failure of immunosuppressive mechanisms. Individuals (14-30 years of age) from an agricultural village in the Nile Delta were selected for study: 12 were uninfected, 9 had S. mansoni infection and hepatosplenomegaly (mean fecal egg excretion 1267 +/- 197 eggs/g), 32 were infected but lacked hepatosplenomegaly (1142 +/- 79 eggs/g). The ratio of OKT4 helper/OKT8 suppressor cells in PBMC was increased in the group with hepatosplenomegaly to 2.7 +/- 0.3 compared to a ratio of 1.7 +/- 0.1 (p less than 0.01) in uninfected subjects; in contrast, this ratio was reduced in infected subjects without hepatosplenomegaly to 1.4 +/- 0.1 (p less than 0.05). Schistosome antigen-induced [3H]thymidine incorporation in PBMC was similar in infected subjects, with hepatosplenomegaly (3329 +/- 738 cpm) and without (5837 +/- 1009 cpm, p greater than 0.01). However, depletion of suppressor adherent cells significantly increased the responses only in the group lacking organomegaly (14,028 +/- 1,683 cpm, p less than 0.001). Thus, among subjects with S. mansoni infection, those with hepatosplenomegaly are distinctive in their failure to develop an immunosuppressive balance of T lymphocyte subpopulations and in the absence of functional adherent suppressor cells.