Peterson Sara Heil, Nardelli Dean T, Warner Thomas F, Callister Steven M, Torrealba Jose R, Schell Ronald F
University of Wisconsin, Wisconsin State Laboratory of Hygiene, Department of Bacteriology, and Department of Pathology, Veterans Administration Hospital, Madison, WI 53706, USA.
Clin Vaccine Immunol. 2007 May;14(5):510-7. doi: 10.1128/CVI.00005-07. Epub 2007 Mar 14.
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.
为阐明莱姆关节炎的发病机制已付出了巨大努力。我们聚焦于p19，一种细胞周期调节分子，因为已知它可抑制可能与关节炎诱导有关的T淋巴细胞的细胞周期分裂。我们发现，抗p19抗体治疗增强了在接种伯氏疏螺旋体疫苗并受到比氏疏螺旋体攻击的小鼠胫跗关节处正常检测到的炎症反应。具体而言，抗p19抗体治疗加剧了滑膜和滑膜下组织内的炎症严重程度。此外，抗p19抗体治疗导致软骨和骨骼严重侵蚀并伴有踝关节破坏。另外，对接种伯氏疏螺旋体疫苗并受到攻击的小鼠进行抗p19抗体治疗增强了杀螺旋体抗体反应，尤其是针对疫苗株的反应。抗p19抗体的这些新活性表明，p19可能是治疗莱姆关节炎的一个重要治疗靶点。
