Nakamura K, Kashiwazaki S, Takagishi K, Tsukamoto Y, Morohoshi Y, Nakano T, Kimura M
Department of Biochemistry, Kitasato University School of Medicine, Kanagawa, Japan.
Arthritis Rheum. 1991 Feb;34(2):171-9. doi: 10.1002/art.1780340207.
Histopathologic studies and radiographic analysis revealed that male New Zealand black/KN (NZB/KN) mice develop degenerative polyarthritis in the joints of the forepaw and hindpaw beginning at age 2 months. Deposits of autoantibodies were observed on proliferating collagen fibers, nuclei of chondrocytes, and epidermal cells. Increases in the frequency of positivity for rheumatoid factor and anti-type II collagen antibodies and in the level of serum oxidation activity were noted in these mice. The joint disease in male NZB/KN mice was transferable to female NZB/KN mice and male BALB/c mice by intraperitoneal injection of spleen cells from the male NZB/KN mice. This animal model of arthritis will be extremely useful for analyzing not only the pathogenesis of rheumatoid arthritis, but also new strategies for its treatment, since NZB/KN mice, unlike MRL/lpr mice, do not develop severe lupus nephritis or lymph-adenopathy, and therefore have a longer survival period.
组织病理学研究和影像学分析显示,雄性新西兰黑/KN(NZB/KN)小鼠从2个月大开始在前爪和后爪关节出现退行性多关节炎。在增殖的胶原纤维、软骨细胞核和表皮细胞上观察到自身抗体沉积。这些小鼠的类风湿因子和抗II型胶原抗体阳性频率以及血清氧化活性水平均有所增加。通过腹腔注射雄性NZB/KN小鼠的脾细胞,雄性NZB/KN小鼠的关节疾病可转移至雌性NZB/KN小鼠和雄性BALB/c小鼠。这种关节炎动物模型不仅对于分析类风湿关节炎的发病机制极其有用,而且对于其治疗新策略也非常有用,因为与MRL/lpr小鼠不同,NZB/KN小鼠不会发生严重的狼疮性肾炎或淋巴结病,因此生存期更长。