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Journal of Clinical Microbiology, February 2005, p. 850-856, Vol. 43, No. 2
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.2.850-856.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis

Elizabeth S. Raveche,¹ Steven E. Schutzer,^1* Helen Fernandes,¹ Helen Bateman,¹ Brian A. McCarthy,¹ Steven P. Nickell,² and Madeleine W. Cunningham³

Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey,¹ Department of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, New Mexico,² University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma³

Received 2 January 2004/ Returned for modification 29 March 2004/ Accepted 5 September 2004

We investigated the possibility that manifestations of Lyme disease in certain hosts, such as arthritis and carditis, may be autoimmunity mediated due to molecular mimicry between the bacterium Borrelia burgdorferi and self-components. We first compared amino acid sequences of Streptococcus pyogenes M protein, a known inducer of antibodies that are cross-reactive with myosin, and B. burgdorferi and found significant homologies with OspA protein. We found that S. pyogenes M5-specific antibodies and sera from B. burgdorferi-infected mice reacted with both myosin and B. burgdorferi proteins by Western blots and enzyme-linked immunosorbent assay. To investigate the relationship between self-reactivity and the response to B. burgdorferi, NZB mice, models of autoimmunity, were infected. NZB mice infected with B. burgdorferi developed higher degrees of joint swelling and higher anti-B. burgdorferi immunoglobulin M cross-reactive responses than other strains with identical major histocompatibility complex (DBA/2 and BALB/c). These studies reveal immunological cross-reactivity and suggest that B. burgdorferi may share common epitopes which mimic self-proteins. These implications could be important for certain autoimmunity-susceptible individuals or animals who become infected with B. burgdorferi.

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* Corresponding author. Mailing address: Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, MSB E543, 185 S. Orange Ave., Newark, NJ 07103. Phone: (973) 972-4872. Fax: (801) 383-8534. E-mail: schutzer{at}umdnj.edu.

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Journal of Clinical Microbiology, February 2005, p. 850-856, Vol. 43, No. 2
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.2.850-856.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

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