Abstract
The chronic musculskeletal and nervous system symptoms that persist after Lyme disease infection are believed to be caused by an autoimmune reaction triggered by B. burgdorferi. A new technique should allow us to identify the self-reactive T cells and antigen epitopes involved (1375–1382).
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 12 print issues and online access
$189.00 per year
only $15.75 per issue
Rent or buy this article
Get just this article for as long as you need it
$39.95
Prices may be subject to local taxes which are calculated during checkout
References
Hemmer, B, et al. Identification of candidate T-cell epitopes and molecular mimics in chronic Lyme disease. Nature Med. 5, 1375–1382 (1999).
Hu, L.T. & Klempner, M.S. Host pathogen interactions and the immunopathogenesis of Lyme disease. J. Clin. Immunol. 17, 354–365 (1997).
Nocton, J.J., Dressler, F., Rutledge, B.J., Persing, D.H. & Steere, A.C. Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis. N. Engl. J. Med. 330, 229– 234 (1994).
Steere, A.C. & Baxter-Lowe, L.A. Association of chronic, treatment resistant Lyme arthritis with rheumatoid arthritis (RA) alleles. Arthritis Rheum. 41, S81 (1998 ).
Gross, D.M., et al. Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis. Science 281, 703– 706 (1998).
Wucherpfennig, K.W. & Strominger, J.L. Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein. Cell 80, 695–705 (1995).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Klempner, M., Huber, B. Is it thee or me?—autoimmunity in Lyme disease. Nat Med 5, 1346–1347 (1999). https://doi.org/10.1038/70907
Issue Date:
DOI: https://doi.org/10.1038/70907
