LYME-DISEASE - A REVIEW OF ASPECTS OF ITS IMMUNOLOGY AND IMMUNOPATHOGENESIS

Lyme disease, caused by Borrelia burgdorferi, causes a multisystem inf lammatory 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 i llness are relieved by antibiotic therapy. A complex interaction betwe en spirochete and immune systems of a number of mammalian hosts, in hu man 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 bas ed on molecular mimicry may play a role in the pathogenesis of Lyme di sease. Humoral immunity plays a protective role, prompting interest in vaccine development. Significant variation in certain of the outer su rface proteins suggests that multiple proteins, peptides, or chimeric vaccines may be needed to provide a sufficiently broad humoral protect ive response.