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Clinical and Diagnostic Laboratory Immunology, September 2002, p. 1095-1101, Vol. 9, No. 5
1071-412X/02/$04.00+0 DOI: 10.1128/CDLI.9.5.1095-1101.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Jani R. Jensen,1,2 Steven M. Callister,4 David J. DeCoster,1,2 and Ronald F. Schell1,2,3*
Wisconsin State Laboratory of Hygiene,1 Departments of Medical Microbiology and Immunology,2 Bacteriology, University of Wisconsin, Madison, Wisconsin 53706,3 Microbiology Research Laboratory and Department of Infectious Diseases, Gundersen Lutheran Medical Center, La Crosse, Wisconsin 546014
Received 5 April 2002/ Returned for modification 17 May 2002/ Accepted 3 June 2002
The ability of a Lyme borreliosis vaccine to induce and maintain sustained levels of borreliacidal antibody is necessary for prolonged protection against infection with Borrelia burgdorferi. Vaccination against infection with B. burgdorferi could be improved by determining the mechanism(s) that influences the production of protective borreliacidal antibody. Borreliacidal antibody was inhibited in cultures of lymph node cells obtained from C3H/HeJ mice vaccinated with formalin-inactivated B. burgdorferi and cultured with macrophages and B. burgdorferi and treated with recombinant gamma interferon (rIFN-
). The suppression of production of outer surface protein A (OspA) borreliacidal antibody by rIFN-
was not affected by the time of treatment. In addition, treatment with rIFN-
inhibited the production of other anti-B. burgdorferi antibodies. By contrast, treatment of cultures of immune lymph node cells with anti-IFN-
marginally increased the production of borreliacidal antibody and enhanced the production of other antibodies directed against B. burgdorferi. These results show that IFN-
does not play a major role in the production of anti-OspA borreliacidal antibody. Additional studies are needed to determine which cytokine(s) will enhance production of borreliacidal antibody.
Present address: Path Lab, Inc., Portsmouth, NH 03801.
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