TY - JOUR
T1 - Immunoglolulin E synthesis in parasite infection
AU - Ishizaka, Teruko
AU - Urban, Joseph
AU - Takatsu, Kiyoshi
AU - Ishizaka, Kimishige
N1 - Funding Information:
From the Department of Medicine and Microbiology, of Medicine at The Good Samaritan Hospital. Supported by Research grant GB 41443 from National Science Foundation, and a grant from the John A. Hartford Foundation, Inc. This paper is Publication No. 227 from the O’Neill Laboratories at the Good Samaritan Hospital. Presented at the Annual Postgraduate Course of the American Academy of Allergy, March 6, 1976. Received for publication May 7, 1976. Accepted for publication May 7, 1976. Reprint requests to: Dr. Teruko Ishizaka, The Johns Hopkins University School of Medicine, 5601 Loch Raven Blvd., Baltimore, Md. 21239. “Postdoctoral trainee supported by Training Grant No. TOl-AI-00423 from the United States Public Health Service.
PY - 1976/10
Y1 - 1976/10
N2 - 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 thymectomised 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 that 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.
AB - 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 thymectomised 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 that 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.
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U2 - 10.1016/0091-6749(76)90196-2
DO - 10.1016/0091-6749(76)90196-2
M3 - Article
C2 - 1085781
AN - SCOPUS:0017199032
SN - 0091-6749
VL - 58
SP - 523
EP - 538
JO - The Journal of allergy and clinical immunology
JF - The Journal of allergy and clinical immunology
IS - 4
ER -