Cellular and molecular aspects of Lyme arthritis

Lyme disease is a multisystem illness initiated upon infection with the spi rochete Borrelia burgdorferi. Whereas the majority of patients who develop Lyme arthritis may be successfully treated with antibiotic therapy, about 1 0% go on to develop arthritis which persists for months to years, despite a ntibiotic therapy. Development of what we have termed treatment-resistant L yme arthritis has previously been associated with both the presence of part icular major histocompatibility complex class II alleles and immunoreactivi ty to the spriochetal outer surface protein A (OspA). Recently, we showed t hat patients with treatment-resistant Lyme arthritis, but not patients with other for-ms of arthritis, generate synovial fluid T cell responses to an immunodominant epitope of OspA and a highly homologous region of the human- lymphocyte-function-associated antigen-1 alpha (L), chain. Identification o f a bacterial antigen capable of propagating an autoimmune response against a self-antigen provides a model of molecular mimicry in the pathogenesis o f treatment-resistant Lyme arthritis.