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Clin Vaccine Immunol. 2007 May;14(5):510-7. Epub 2007 Mar 14.

Anti-p19 antibody treatment exacerbates lyme arthritis and enhances borreliacidal activity.

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University of Wisconsin, Wisconsin State Laboratory of Hygiene, Department of Bacteriology, and Department of Pathology, Veterans Administration Hospital, Madison, WI 53706, USA.


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.

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