Haakenstad A O
J Immunol. 1987 Jun 15;138(12):4192-9.
The solubilization and removal of defined glomerular immune complex deposits by excess antigen was examined in NZB/W female mice. Glomerular deposits were induced by administering preformed immune complexes to young (2 to 4 mo) mice before they naturally acquired deposits from endogenous disease and to old (7 mo) mice with deposits from naturally acquired disease. The administration of excess antigen specifically removed deposits of preformed immune complexes in both groups. This was associated with a reduction in circulating large latticed complexes containing more than two antigen and two antibody molecules (greater than Ag2Ab2). Established deposits in old mice therefore did not interfere with removal of newly induced deposits of preformed immune complexes. Glomerular deposits were also induced in young mice by a chronic human serum albumin (HSA) immune complex model. The antigen in immune deposits induced by 2 wk of chronic antigen administration was solubilized and was removed within 48 hr of administering excess antigen. Circulating antibodies to the antigen were also reduced by excess antigen. Glomerular deposits of mouse immunoglobulin and complement were not significantly reduced by excess antigen but remained more intense than in mice of comparable age given preformed complexes. Thus deposits of other antigen antibody systems and possibly endogenous disease were induced by the chronic HSA immune complex model in NZB/W mice. However, defined antigen deposits within deposits containing multiple antigen antibody systems can clearly be removed by administering excess antigen.
在NZB/W雌性小鼠中研究了用过量抗原溶解和清除特定肾小球免疫复合物沉积物的情况。通过向年轻(2至4个月)小鼠在其自然获得内源性疾病沉积物之前以及向患有自然获得性疾病沉积物的老年(7个月)小鼠给予预先形成的免疫复合物来诱导肾小球沉积物。给予过量抗原可特异性清除两组中预先形成的免疫复合物沉积物。这与循环中含有超过两个抗原和两个抗体分子(大于Ag2Ab2)的大晶格复合物减少有关。因此,老年小鼠中已形成的沉积物不会干扰新诱导的预先形成的免疫复合物沉积物的清除。还通过慢性人血清白蛋白(HSA)免疫复合物模型在年轻小鼠中诱导肾小球沉积物。通过2周慢性抗原给药诱导的免疫沉积物中的抗原在给予过量抗原后48小时内被溶解并清除。过量抗原也降低了针对该抗原的循环抗体。过量抗原并未显著减少小鼠免疫球蛋白和补体的肾小球沉积物,但仍比给予预先形成复合物的同龄小鼠中的沉积物更强烈。因此,慢性HSA免疫复合物模型在NZB/W小鼠中诱导了其他抗原抗体系统的沉积物以及可能的内源性疾病。然而,通过给予过量抗原可以清楚地清除含有多种抗原抗体系统的沉积物中的特定抗原沉积物。