Failure of malaria vaccination in mice born to immune mothers.
Female BALB/c mice were vaccinated against blood stage P. yoelii (17XL strain), infected 2 weeks later and after recovery mated to normal C57B1/6 males. Control matings were with normal BALB/c females. The (C57B1/6 x BALB/c)F1 progeny were vaccinated at 4, 6, 8 or 10 weeks of age and infected 2 weeks later with lethal P. yoelii. All control mice were fully protected, but in the offspring of immune mothers mortality was 100, 87, 50, and 0% respectively. Mice in which the protective effect of vaccination had been abolished showed greatly reduced specific IgG and delayed hypersensitivity (DH) responses to challenge with parasite antigen. Results indicate that this failure of vaccination is due to the transmission of maternal IgG to the offspring which acts to suppress both priming by the vaccine and the generation of specific T helper cells involved in IgG production, as measured by the response to TNP-P. yoelii.
D000818:Animals; D000906:Antibodies / Q000032:analysis; D005260:Female; D007111:Immunity, Cellular; D007112:Immunity, Maternally-Acquired; D007074:Immunoglobulin G / Q000276:immunology; D008288:Malaria / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D010961:Plasmodium / Q000276:immunology; D011247:Pregnancy; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D014611:Vaccination; D014612:Vaccines / Q000276:immunology
D000906:Antibodies; D007074:Immunoglobulin G; D014612:Vaccines