Lyme disease: a review of aspects of its immunology and immunopathogenesis.
Lyme disease, caused by Borrelia burgdorferi, causes a multisystem inflammatory ailment, although the precise means of tissue damage are not well understood. It is clear that the organism is present at the site of inflammation in many organs and that many of the features of the illness are relieved by antibiotic therapy. A complex interaction between spirochete and immune systems of a number of mammalian hosts, in human disease and animal models, has been described. It is clear that T cells and macrophages are intimately associated with the pathogenesis of arthritis and that immune mechanisms are involved in other aspects of disease. Inflammation directed at persistence of Borrelial antigens is a plausible explanation for persisting arthritis. Autoimmunity based on molecular mimicry may play a role in the pathogenesis of Lyme disease. Humoral immunity plays a protective role, prompting interest in vaccine development. Significant variation in certain of the outer surface proteins suggests that multiple proteins, peptides, or chimeric vaccines may be needed to provide a sufficiently broad humoral protective response.
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Division of Rheumatology and Connective Tissue Research, UMDNJ-Robert Wood Johnson Medical School, New Brunswick 08903, USA.
D000818:Animals; D001096:Arachnid Vectors / Q000382:microbiology; D015551:Autoimmunity; D015748:Borrelia burgdorferi Group / Q000472:pathogenicity; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D008193:Lyme Disease / Q000209:etiology* / Q000276:immunology* / Q000503:physiopathology; D008214:Lymphocytes / Q000276:immunology; D010586:Phagocytes / Q000502:physiology; D013987:Ticks / Q000382:microbiology
D016207:Cytokines; D005609:Free Radicals