Abstract
Considerable effort has been made to elucidate the mechanism of Lyme arthritis. We focused on p19, a cell cycle-regulating molecule, because it is known to inhibit cell cycle division of T lymphocytes which may be responsible for the induction of arthritis. We show that anti-p19 antibody treatment enhances the inflammatory response normally detected at the tibiotarsal joints of Borrelia burgdorferi-vaccinated and Borrelia bissettii challenged mice. Specifically, anti-p19 antibody treatment augmented the severity of inflammation within the synovial and subsynovial tissue. Moreover, treatment with anti-p19 antibody caused severe erosion of cartilage and bone with ankle joint destruction. In addition, anti-p19 antibody treatment of Borrelia-vaccinated and -challenged mice enhanced the borreliacidal antibody response, especially against the vaccine isolate. The novel activities of anti-p19 antibody show that p19 may be an important therapeutic site for the treatment of Lyme arthritis.
Original language | English (US) |
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Pages (from-to) | 510-517 |
Number of pages | 8 |
Journal | Clinical and Vaccine Immunology |
Volume | 14 |
Issue number | 5 |
DOIs | |
State | Published - May 2007 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Clinical Biochemistry
- Microbiology (medical)