Lambert P H, Dixon F J
J Exp Med. 1968 Mar 1;127(3):507-22. doi: 10.1084/jem.127.3.507.
The development of glomerulonephritis in NZB/W mice is closely related to the formation of antinuclear, particularly anti-DNA, antibodies. The developing inflammatory glomerular lesions are characterized by the deposition of gammaG- and beta(1C)-globulins plus DNA and possibly other nuclear antigens, presumably as complexes, in a granular to lumpy pattern along the capillary walls and in the mesangia. Elution studies revealed the gammaG-globulin in the glomeruli to be largely gammaG(2A)-type antibody to soluble nuclear antigens. Enhancement of the antinuclear antibody response by active immunization of young NZB/W mice with DNA-methylated BSA hastens the development and increases the severity of the glomerulonephritis. Similarly, injections of soluble DNA into NZB/W mice with circulating anti-DNA antibodies but with as yet little nephritis causes rapid progression of nephritis.
NZB/W小鼠肾小球肾炎的发展与抗核抗体，特别是抗DNA抗体的形成密切相关。正在发展的炎症性肾小球病变的特征是γG和β(1C)球蛋白以及DNA和可能的其他核抗原（推测为复合物）以颗粒状至块状的形式沿着毛细血管壁和系膜沉积。洗脱研究表明，肾小球中的γG球蛋白主要是针对可溶性核抗原的γG(2A)型抗体。用DNA甲基化牛血清白蛋白主动免疫年轻的NZB/W小鼠可增强抗核抗体反应，加速肾小球肾炎的发展并增加其严重程度。同样，向具有循环抗DNA抗体但尚无明显肾炎的NZB/W小鼠注射可溶性DNA会导致肾炎迅速进展。
