Immunoglobulin E synthesis in parasite infection.

The infection of rats with Nippostrongylus brasiliensis (Nb) larvae enhanced IgE synthesis prior to the formation of IgE antibody specific for parasite antigens. As early as the eighth to tenth day of infection, IgE-bearing lymphocytes appeared in lymph nodes and spleen. At this time, even bone marrow contained IgE-bearing blast cells. The IgE-forming plasma cells were detected in the lymph nodes and spleen at the tenth day and their number reached maximum at the fourteenth day. The proliferation of IgE-bearing lymphocytes in the lymphoid tissues was observed in neonatally thymectomized animals, indicating that T cells are not essential for the development of IgE-B cells in the infected animals. It appears, however, that T cells are involved in the differentiation of IgE-B cells to IgE-forming plasma cells. Nonspecific proliferation of IgE-B cells and their differentiation to IgE-forming plasma cells may explain potentiation of IgE antibody formation against unrelated antigens after infection with N. brasiliensis (Nb). It was also found that T cells specific for parasite antigens were primed by infection with Nb. Evidence was obtained tht Nb-specific T cells raised by the infection collaborated with hapten-specific IgE-B cells and IgG-B cells for the secondary antihapten antibody responses. By contrast, T cells primed by immunization with parasite antigen included in alum exerted the helper function for IgG antibody response but failed to collaborate with IgE-B cells. Dissociation between the helper function for IgE and IgG antibody response indicated that parasite infection generated a favorable condition for priming T cells for the IgE antibody response.