| First Author | Iliopoulou BP | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 12 | Pages | 8076-82 |
| PubMed ID | 18056348 | Mgi Jnum | J:155039 |
| Mgi Id | MGI:4412171 | Doi | 10.4049/jimmunol.179.12.8076 |
| Citation | Iliopoulou BP, et al. (2007) CD28 deficiency exacerbates joint inflammation upon Borrelia burgdorferi infection, resulting in the development of chronic Lyme arthritis. J Immunol 179(12):8076-82 |
| abstractText | 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. |
