Izui S, McConahey P J, Theofilopoulos A N, Dixon F J
J Exp Med. 1979 May 1;149(5):1099-116. doi: 10.1084/jem.149.5.1099.
Endogenous retroviral gp70 was investigated as a participant in the pathogenesis of a lupus-like disease that spontaneously develops in four kinds of mice (NZB, NZB x W MRL/1, and male BXSB). Sera from these strains contain a heavy form of gp 70 that varies in sedimentation rates from 9S to 19S in sucrose density gradient analysis and appears with the onset of disease and persists throughout its course. Immunologically normal strains of mice do not develop rapidly sedimenting gp70 by 8-10 mo of life. The fact that the heavy gp70 is selectively absorbed with anti-IgG antibodies or with Staphylococcus aureus protein A suggests that it is complexed with antibodies. The incidence and quantities of these gp70 ICs rise with the progression of disease in all strains with lupus. These findings suggest that Ig-complexed heavy gp70 may be involved in the pathogenesis of glomerulonephritis of mice with SLE.
内源性逆转录病毒糖蛋白70(gp70)被作为一种参与在四种小鼠(新西兰黑鼠、新西兰黑鼠×W MRL/1杂交鼠以及雄性BXSB小鼠)中自发产生的狼疮样疾病发病机制的因素进行了研究。这些品系小鼠的血清中含有一种重形式的gp70,在蔗糖密度梯度分析中其沉降速率在9S至19S之间变化,并且在疾病发作时出现并在整个病程中持续存在。免疫正常的小鼠品系在8至10月龄时不会产生快速沉降的gp70。重gp70能被抗IgG抗体或金黄色葡萄球菌蛋白A选择性吸收,这一事实表明它与抗体形成了复合物。在所有患狼疮的品系中,这些gp70免疫复合物(ICs)的发生率和数量随着疾病的进展而增加。这些发现表明,Ig复合的重gp70可能参与了系统性红斑狼疮(SLE)小鼠肾小球肾炎的发病机制。