Cellular and Molecular Life Sciences CMLS

, Volume 57, Issue 11, pp 1562–1569

Cellular and molecular aspects of Lyme arthritis

  • D.M. Gross
  • B.T. Huber

DOI: 10.1007/PL00000641

Cite this article as:
Gross, D. & Huber, B. CMLS, Cell. Mol. Life Sci. (2000) 57: 1562. doi:10.1007/PL00000641
  • 50 Downloads

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-1αL 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.

Key words. Lyme disease; arthritis; autoimmunity; molecular mimicry; OspA. 

Copyright information

© Birkhäuser Verlag Basel, 2000

Authors and Affiliations

  • D.M. Gross
    • 1
  • B.T. Huber
    • 1
  1. 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

Personalised recommendations