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Science 31 July 1998:
Vol. 281. no. 5377, pp. 703 - 706
DOI: 10.1126/science.281.5377.703
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Reports

Identification of LFA-1 as a Candidate Autoantigen in Treatment-Resistant Lyme Arthritis

Dawn M. Gross, Thomas Forsthuber, Magdalena Tary-Lehmann, Carey Etling, Kouichi Ito, Zoltan A. Nagy, Jodie A. Field, Allen C. Steere, Brigitte T. Huber

Treatment-resistant Lyme arthritis is associated with immune reactivity to outer surface protein A (OspA) of Borrelia burgdorferi, the agent of Lyme disease, and the major histocompatibility complex class II allele DRB1*0401. The immunodominant epitope of OspA for T helper cells was identified. A homology search revealed a peptide from human leukocyte function-associated antigen-1 (hLFA-1) as a candidate autoantigen. Individuals with treatment-resistant Lyme arthritis, but not other forms of arthritis, generated responses to OspA, hLFA-1, and their highly related peptide epitopes. Identification of the initiating bacterial antigen and a cross-reactive autoantigen may provide a model for development of autoimmune disease.

D. M. Gross and B. T. Huber, Department of Pathology, Tufts University, Boston, MA 02111 USA. T. Forsthuber, M. Tary-Lehmann, C. Etling, Department of Pathology, Case Western Reserve University, Cleveland, OH 44106-4943, USA. K. Ito and Z. A. Nagy, Department of Immunology, Hoffmann-La Roche, Nutley, NJ 07110, USA. J. A. Field and A. C. Steere, Department of Rheumatology, New England Medical Center, Boston, MA 02111, USA.

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PNAS 96, 5340-5342
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The Immunoglobulin (IgG) Antibody Response to OspA and OspB Correlates with Severe and Prolonged Lyme Arthritis and the IgG Response to P35 Correlates with Mild and Brief Arthritis.
E. Akin, G. L. McHugh, R. A. Flavell, E. Fikrig, and A. C. Steere (1999)
Infect. Immun. 67, 173-181
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Possible Cause of Treatment-Resistant Lyme Arthritis.
(1998)
Journal Watch Infectious Diseases 1998, 2
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Direct enumeration of Borrelia-reactive CD4 T cells ex vivo by using MHC class II tetramers.
A. L. Meyer, C. Trollmo, F. Crawford, P. Marrack, A. C. Steere, B. T. Huber, J. Kappler, and D. A. Hafler (2000)
PNAS 97, 11433-11438
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