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肾小球肾炎中的肾小球抗原。

Glomerular antigens in glomerulonephritis.

作者信息

Neale T J, Wilson C B

出版信息

Springer Semin Immunopathol. 1982;5(3):221-49. doi: 10.1007/BF01892087.

Abstract

Ideas on the immunopathogenesis of glomerulonephritis are evolving to embrace a concept of a dynamic and constantly fluctuating involvement of immune reactants in the production of glomerular inflammation. The glomerulus should be regarded as a template around which the antibody-induced inflammatory events that constitute glomerulonephritis are initiated. Such lesions may be produced by direct antibody attack on glomerular antigens of either intrinsic structural or "planted" type, as discussed in this review, or by the deposition of circulating soluble immune complexes containing extraglomerular antigens. These mechanisms are not mutually exclusive and both may play a role in some situations. Intrinsic glomerular antigens are being increasingly better defined as to site, structure, function, and experimental animal models of spontaneous and induced glomerular injury resulting from direct antibody binding to nonclassic GBM capillary wall antigens are available for study. Similar nonclassic GBM antigens are likely to be found of importance in man. Anti-GBM antibody-induced glomerulonephritis continues to be the best understood example of direct attack on the glomerulus by antibody, and its nephritogenic noncollagenous GBM antigenic constituents are being characterized. The incorporation of extraneous substances as "planted" antigens within glomerular structures is now recognized in experimental animal models, and there is suggestive evidence to support the concept in man. Emphasis needs to be placed on the continuing interplay of free antibody and antigen with deposited reactants which, together with complement components, modulate the quality and quantity of the glomerular immune deposits.

摘要

关于肾小球肾炎免疫发病机制的观点正在不断演变,以接受这样一个概念,即免疫反应物在肾小球炎症产生过程中发挥动态且持续波动的作用。肾小球应被视为一个模板,围绕该模板引发构成肾小球肾炎的抗体诱导性炎症事件。如本综述所讨论的,此类病变可能由抗体直接攻击内在结构型或“植入”型的肾小球抗原产生,或者由含有肾小球外抗原的循环可溶性免疫复合物沉积所致。这些机制并非相互排斥,在某些情况下可能都发挥作用。随着内在肾小球抗原在部位、结构、功能方面的定义日益清晰,针对由抗体直接结合非经典肾小球基底膜(GBM)毛细血管壁抗原所导致的自发性和诱发性肾小球损伤的实验动物模型也可供研究。类似的非经典GBM抗原在人类中可能也具有重要意义。抗GBM抗体诱导的肾小球肾炎仍然是抗体直接攻击肾小球的最易于理解的例子,其致肾炎的非胶原性GBM抗原成分正在得到表征。在实验动物模型中,现已认识到将外来物质作为“植入”抗原纳入肾小球结构的现象,并且有提示性证据支持人类中的这一概念。需要强调的是,游离抗体和抗原与沉积反应物之间持续的相互作用,它们与补体成分一起,调节肾小球免疫沉积物的质量和数量。

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