Cellular and molecular aspects of Lyme arthritis |
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Authors: | Gross D M Huber B T |
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Institution: | (1) Department of Pathology, Program in Immunology, Sackler School of Biomedical Sciences, Tufts University School of Medicine, Boston (Massachusetts 02111, USA), Fax +1 617 636 0449, e-mail: bhuber@opal.tufts.edu , US |
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Abstract: | Lyme disease is a multisystem illness initiated upon infection with the spirochete Borrelia burgdorferi. Whereas the majority of patients who develop Lyme arthritis may be successfully treated with antibiotic therapy, about 10%
go on to develop arthritis which persists for months to years, despite antibiotic therapy. Development of what we have termed
treatment-resistant Lyme arthritis has previously been associated with both the presence of particular major histocompatibility
complex class II alleles and immunoreactivity to the spriochetal outer surface protein A (OspA). Recently, we showed that
patients with treatment-resistant Lyme arthritis, but not patients with other forms of arthritis, generate synovial fluid
T cell responses to an immunodominant epitope of OspA and a highly homologous region of the human-lymphocyte-function-associated
antigen-1α
L chain. Identification of a bacterial antigen capable of propagating an autoimmune response against a self-antigen provides
a model of molecular mimicry in the pathogenesis of treatment-resistant Lyme arthritis.
Received 21 December 1999; received after revision 10 April 2000; accepted 11 April 2000 |
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Keywords: | , Lyme disease, arthritis, autoimmunity, molecular mimicry, OspA, |
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