RT Journal Article
SR Electronic
T1 Evidence of <em>Borrelia</em> 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.