Fu Yuyang, Du Yong, Mohan Chandra
Department of Internal Medicine (Rheumatology) and Immunology, University of Texas Southwestern Medical School, Y8.204, 5323 Harry Hines Boulevard, Dallas, TX 75390-8884, USA.
Clin Immunol. 2007 Aug;124(2):109-18. doi: 10.1016/j.clim.2007.05.007.
Lupus nephritis is an immune-mediated disease, where antibodies and T cells both play pathogenic roles. Since spontaneous lupus nephritis in mouse models takes 6-12 months to manifest, there is an urgent need for a mouse model that can be used to delineate the pathogenic processes that lead to immune nephritis, over a quicker time frame. We propose that the experimental anti-glomerular basement membrane (GBM) disease model might be a suitable tool for uncovering some of the molecular steps underlying lupus nephritis. This article reviews the current evidence that supports the use of the experimental anti-GBM nephritis model for studying spontaneous lupus nephritis. Importantly, out of about 25 different molecules that have been specifically examined in the experimental anti-GBM model and also spontaneous lupus nephritis, all influence both diseases concordantly, suggesting that the experimental model might be a useful tool for unraveling the molecular basis of spontaneous lupus nephritis. This has important clinical implications, both from the perspective of genetic susceptibility as well as clinical therapeutics.
狼疮性肾炎是一种免疫介导的疾病，抗体和T细胞在其中均发挥致病作用。由于小鼠模型中的自发性狼疮性肾炎需要6至12个月才能显现，因此迫切需要一种能够在更短时间内用于描绘导致免疫性肾炎的致病过程的小鼠模型。我们认为，实验性抗肾小球基底膜（GBM）疾病模型可能是揭示狼疮性肾炎潜在分子机制的合适工具。本文综述了支持使用实验性抗GBM肾炎模型研究自发性狼疮性肾炎的现有证据。重要的是，在实验性抗GBM模型和自发性狼疮性肾炎中专门检测的约25种不同分子中，所有这些分子对两种疾病的影响都是一致的，这表明该实验模型可能是阐明自发性狼疮性肾炎分子基础的有用工具。这从遗传易感性以及临床治疗的角度来看都具有重要的临床意义。
