自从Bielschowsky 等人制成新西兰黑鼠(NZB)做为自身免疫病的动物模型,至今约25年间,新西兰鼠(NZ)成了人全身性红斑狼疮(SLE)的研究对比中心。如同人SLE 那样,NZ鼠也能产生抗DNA 抗体、胸腺细胞毒性自身抗体(NTA)等自身抗体,出现高免疫球蛋白血症、狼疮性肾炎等各种SLE 病症。许多研究结果表明,这些SLE 病症的发生是受各种独立的多数基因控制的。为了查明各个基因以怎样的机制引起各种免疫异常,世界各主要研究室正在分离各个基因,建立具有重新近交小鼠和同类小鼠品系,进行更深入的研究。 Since Bielschowsky et al. Have made New Zealand black rat (NZB) an animal model of autoimmune disease, New Zealand rat (NZ) has been the research center of human systemic lupus erythematosus (SLE) for about 25 years. As with human SLE, NZ mice also develop autoantibodies such as anti-DNA antibodies and thymus cytotoxic autoantibodies (NTAs), and develop various SLE conditions such as hypercholesterolemia and lupus nephritis. Many studies have shown that the occurrence of these SLE disorders is controlled by a majority of independent genes. In order to find out the mechanism by which each gene causes a variety of immune abnormalities, major research laboratories in the world are isolating individual genes, establishing strains with reconstituted mice and their homologous mice, and conducting further studies.