Monoclonal antibodies specific for the outer surface protein A (OspA) of Borrelia burgdorferi prevent Lyme borreliosis in severe combined immunodeficiency (scid) mice.

U E Schaible(Max Planck Institute of Immunobiology and Epigenetics), Michael D. Kramer(Max Planck Institute of Immunobiology and Epigenetics), Klaus Eichmann(Max Planck Institute of Immunobiology and Epigenetics), Manuel Modolell(Max Planck Institute of Immunobiology and Epigenetics), C Muşeţeanu(Max Planck Institute of Immunobiology and Epigenetics), Markus M. Simon(Max Planck Institute of Immunobiology and Epigenetics)
Proceedings of the National Academy of Sciences
May 1, 1990
Cited by 278Open Access
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Abstract

We have recently shown that viable Borrelia burgdorferi organisms induce a chronic infection associated with arthritis and carditis in severe combined immunodeficiency (scid) mice but not in immunocompetent mice. The disease is similar to that found in patients suffering from Lyme disease. We now show that B. burgdorferi-specific immune mouse sera as well as a monoclonal antibody to the spirochetal outer surface antigen A (31 kDa) but not monoclonal antibodies specific for the 41-kDa antigenic component of the periplasmic flagella are able to prevent (or mitigate) the development of the disease in scid mice when passively transferred at the time of the bacterial inoculation. The identification of a B. burgdorferi-associated protective antigen suggests that the corresponding spirochetal protein should be tested as a vaccine against Lyme disease.


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