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Clinical and Diagnostic Laboratory Immunology, January 2004, p. 35-41, Vol. 11, No. 1
1071-412X/04/$08.00+0 DOI: 10.1128/CDLI.11.1.35-41.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
David J. DeCoster,1,2 Dean T. Nardelli,1,3 Douglas M. England,4,5 Steven M. Callister,6 and Ronald F. Schell1,2,3*
Wisconsin State Laboratory of Hygiene,1 Departments of Medical Microbiology and Immunology,2 Pathology and Laboratory Medicine,4 Bacteriology, University of Wisconsin, Madison, Wisconsin 53706,3 Department of Pathology, Meriter Hospital, Madison, Wisconsin 53715,5 Microbiology Research Laboratory and Department of Infectious Diseases, Gundersen Lutheran Medical Center, La Crosse, Wisconsin 546016
Received 7 August 2003/ Returned for modification 26 September 2003/ Accepted 17 October 2003
Development of a high level of sustained borreliacidal antibody is paramount for maintaining protection against infection with Borrelia burgdorferi. We show that production of borreliacidal antibody can be enhanced by preventing the effects of gamma interferon (IFN-
). When lymph node cells capable of producing borreliacidal antibody were cultured with anti-murine IFN-
, an eightfold increase in borreliacidal antibody production was obtained. However, anti-IFN-
treatment of these cells also enhanced their ability to adaptively induce arthritis. When anti-IFN-
-treated lymph node cells producing borreliacidal antibody were infused into C3H/HeJ mice and the mice were then challenged with B. burgdorferi, the mice developed severe destructive Lyme arthritis. Additional studies are needed to delineate the immune response responsible for the induction of arthritis and production of borreliacidal antibody. These studies are needed to ensure an effective and safe vaccine against infection with B. burgdorferi.
Present address: Medical Science Laboratories, Wauwatosa, WI 53226.
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