Molecular mimicry to Borrelia burgdorferi: pathway to autoimmunity?
Lyme borreliosis is due to infection with the tick-borne spirochete Borrelia burgdorferi, and is associated with persistent infection unless treated with antibiotics. The persistent nature of infection by B. burgdorferi can lead to development of chronic disease, as found in patients infected before recognition of the effectiveness of antibiotic therapy. Much speculation has surrounded the possibility that autoimmune mechanisms are involved in chronic symptoms. In most cases, involvement of autoimmunity in Lyme disease has not received experimental support. The exception is in a small group of patients with chronic arthritis whose abnormal joint symptoms persist after apparent elimination of the bacteria. In this review, the evidence supporting autoimmune mechanisms in Lyme disease will be discussed.
Bolz
Devin D
DD
Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
Weis
Janis J
JJ
D000954:Antigens, Surface / Q000235:genetics / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology*; D001425:Bacterial Outer Membrane Proteins / Q000235:genetics / Q000276:immunology; D001428:Bacterial Vaccines; D025065:Borrelia burgdorferi / Q000276:immunology*; D002908:Chronic Disease; D006801:Humans; D008074:Lipoproteins / Q000235:genetics / Q000276:immunology; D008193:Lyme Disease / Q000276:immunology*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000235:genetics / Q000276:immunology; D018716:Molecular Mimicry / Q000235:genetics / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D000954:Antigens, Surface; D001425:Bacterial Outer Membrane Proteins; D001428:Bacterial Vaccines; D008074:Lipoproteins; D016169:Lymphocyte Function-Associated Antigen-1; C072045:OspA protein