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We investigated the mechanisms of specific immune unresponsiveness to microfilarial antigens. The blood of patients with obvious Brugia malayi infections contains an adherent cell type that specifically suppresses reactions to microfilarial antigens but not to other antigens. In the absence of continued stimulation by parasite antigens, this suppressor cell loses its functional activity after overnight culture in vitro. Furthermore, serums from patients with and without microfilaremia contain factors that also suppress reactions to filarial antigens in vitro. These results suggest that immune unresponsiveness in human beings with patent filarial infections is due to active suppression of immune responses directed against the parasite and not to an intrinsic inability of infected patients to react to parasite antigens.

Immune responses to parasite antigens are much lower in patients with microfilaremia than in persons with other manifestations of brugian filariasis. To determine whether hyporeactivity is associated with changes in populations of lymphocytes that regulate immune responses, we quantitated helper and suppressor T cells in the blood of patients infected with Brugia malayi. Increased numbers of suppressor T cells were present in 15 of 17 patients with microfilaremia and in six of 11 patients with elephantiasis. This increase correlated with hyporeactivity to filarial antigens but not to nonparasite antigens. Removal of suppressor T cells activated in vivo or in vitro improved reactivity to filarial antigens. These results suggest that immunosuppression induced by filarial parasites is a possible mechanism of survival of these organisms in an immunocompetent host.

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To study the pathogenesis of tropical splenomegaly syndrome, we compared immunologic findings in patients from Flores, Indonesia, with those obtained in local residents without splenomegaly and in controls. Villagers with tropical splenomegaly syndrome had markedly elevated levels of total IgM, higher titers of IgM antibodies to Plasmodium vivax, and reduced levels of circulating T lymphocytes. The latter were caused by a decrease in the total number of T cells with the suppressor/cytotoxic phenotype (T8+). Levels of B lymphocytes were similar in all groups. All immunologic abnormalities reverted toward normal in patients treated weekly for 9 to 26 months with chloroquine phosphate. These findings suggest that overproduction of immunoglobulins in patients with tropical splenomegaly syndrome is caused by an imbalance in the normal ratio of helper: suppressor T cells that regulate B-lymphocyte function, and that this imbalance is due to a decrease in suppressor T lymphocytes.