Immunologic mechanisms in Lyme neuroborreliosis: the potential role of autoimmunity and molecular mimicry.

Most of the clinical manifestations of Lyme disease are due to the local presence of the causative agent, Borrelia burgdorferi, in the affected tissues. However, the precise means of tissue damage are not well understood and there is no proof that the organism, live or dead, is always present. An understanding of the complex interaction between the organism, the immune response elicited by the organism, and the host can explain manifestations of the disease and persistence of symptoms and signs after the antibiotic-induced death of the organism. It is possible that dead spirochetes, or fragments thereof may persist and act as a focus of ongoing inflammation. Different immunogenetic types may predispose to different immunologic responses, with distinct clinical outcomes. Vascular changes induced by the infection, either by local infection or the effects of cytokines on the vessel wall, may underlie tissue pathology. Finally, the immune response to B. burgdorferi may elicit the production of antibodies capable of recognizing and damaging or modifying normal host tissues. Only by establishing the mechanisms causing tissue damage in Lyme disease can rational therapeutic strategies be developed. Only by understanding these mechanisms can physicians and patients interpret clinical responses to therapy and accurately appreciate the clinical prognosis.