IMMUNOGLOBULIN E SYNTHESIS IN PARASITE INFECTION

[摘要] The infection of rats with Nippostronglyus brasiliensis (Nb) larvae enhanced IgE [immunoglobulin E] synthesis prior to the formation of IgE antibody specific for parasite antigens. As early as the 8th-10th 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 10th day, and their number reached maximum at the 14th day. The proliferation of IgE-bearing lymphocytes in the lymphoid tissues was observed in neonatally thymectomized animals, indicating that T [thymus-derived] cells are not essential for the development of IgE-B [bone marrow-derived] cells in the infected animals. T cells are apparently 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. basiliensis (Nb). T cells specific for parasite antigens were primed by infection with Nb. 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. T cells primed by immunization with parasite antigen included in alum exerted the helper function for the 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.