Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi (Bb), is a multisystem illness, affecting many organs, such as the heart, the nervous system, and the joints. Months after Bb
infection, approximately 60% of patients experience intermittent arthritic attacks, a condition that in some individuals progresses to chronic joint
inflammation. Although mice develop acute
arthritis in response to Bb
infection, the joint
inflammation clears after 2 wk, despite continuous
infection, only very rarely presenting with chronic
Lyme arthritis. Thus, the lack of an animal system has so far prevented the elucidation of this persistent inflammatory process that occurs in humans. In this study, we report that the majority of Bb-infected CD28-/- mice develop chronic
Lyme arthritis. Consistent with observations in chronic
Lyme arthritis patients, the infected mutant, but not wild-type mice present recurring monoarticular
arthritis over an extended time period, as well as anti-
outer surface protein A of Bb serum titers. Furthermore, we demonstrate that anti-
outer surface protein A Abs develop in these mice only after establishment of chronic
Lyme arthritis. Thus, the Bb-infected CD28-/- mice provide a murine model for studying chronic
Lyme arthritis.