RT Journal Article SR Electronic T1 Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis JF Journal of Clinical Microbiology JO J. Clin. Microbiol. FD American Society for Microbiology SP 850 OP 856 DO 10.1128/JCM.43.2.850-856.2005 VO 43 IS 2 A1 Raveche, Elizabeth S. A1 Schutzer, Steven E. A1 Fernandes, Helen A1 Bateman, Helen A1 McCarthy, Brian A. A1 Nickell, Steven P. A1 Cunningham, Madeleine W. YR 2005 UL http://jcm.asm.org/content/43/2/850.abstract AB 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.