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抗肾小球基底膜自身抗体可加速小鼠狼疮性肾炎。

Murine lupus nephritis is accelerated by anti-glomerular basement membrane autoantibodies.

作者信息

Rudofsky U H

出版信息

Clin Exp Immunol. 1981 Apr;44(1):18-23.

Abstract

We have tested the effect of deposition of non-pathogenic amounts of induced anti-glomerular basement membrane (GBM) autoantibodies on the development of the spontaneous lupus nephritis of female (NZB x NZW) F1 (B x W) mice. Female and male B x W mice were immunized with rabbit renal tubular basement membrane in adjuvant at 2 months of age and their kidneys were examined 35 to 66 days later; control B x W mice were injected with adjuvant only or remained untreated. By immunofluorescent and histopathological criteria, only the 4-month-old female B x W mice with anti-GBM autoantibody deposits had an accelerated onset of lupus nephritis resembling the findings not seen until 6 to 8 months of age in unmanipulated mice. Thus potentially pathogenic amounts of immune complexes are present in young female B x W mice, but these do not deposit in glomeruli until much later in life. Evidently, the anti-GBM autoantibodies modified the glomerular milieu sufficiently to facilitate accelerated immune complex deposition.

摘要

我们已经测试了非致病性剂量的诱导抗肾小球基底膜(GBM)自身抗体的沉积对雌性(NZB×NZW)F1(B×W)小鼠自发性狼疮性肾炎发展的影响。雌性和雄性B×W小鼠在2月龄时用佐剂中的兔肾小管基底膜进行免疫,35至66天后检查它们的肾脏;对照B×W小鼠仅注射佐剂或不进行处理。根据免疫荧光和组织病理学标准,只有具有抗GBM自身抗体沉积的4月龄雌性B×W小鼠狼疮性肾炎发病加速,类似于未处理小鼠直到6至8月龄才出现的表现。因此,年轻雌性B×W小鼠中存在潜在致病性剂量的免疫复合物,但这些复合物直到生命后期才沉积在肾小球中。显然,抗GBM自身抗体充分改变了肾小球环境,以促进免疫复合物的加速沉积。

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The biology and detection of immune complexes.
Adv Immunol. 1979;28:89-220. doi: 10.1016/s0065-2776(08)60800-7.

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