Agostini C, Basso U, Semenzato G
Padua University School of Medicine, Department of Clinical and Experimental Medicine, Italy.
J Clin Immunol. 1998 May;18(3):184-92. doi: 10.1023/a:1020526904867.
Although the etiology of sarcoidosis is still unknown, characteristic morphologic aspects and immunohistological patterns of sarcoid granulomatous lesions suggest that they are the consequence of an exaggerated immunological response against an undefined antigen which persists at different sites of disease involvement. This article reviews the newly emerging hypothesis regarding the molecular bases which drive the development of sarcoid granulomas. The accumulation of Th1 cells represents the pivotal step along the series of events that lead to the formation of granuloma; furthermore, a set of biological mediators of the immune response define immune regulatory networks that may contribute to tissue damage. It is also thought that shifts of the Th1/Th2 networks and alterations in the complex networks between immunocompetent cells and mesenchymal cells may set the stage for the remodeling of tissues surrounding granulomatous lesions.
尽管结节病的病因仍不明确，但结节病肉芽肿性病变的特征性形态学表现和免疫组织学模式提示，它们是针对一种未明确的抗原产生过度免疫反应的结果，该抗原持续存在于疾病累及的不同部位。本文综述了关于驱动结节病肉芽肿形成的分子基础的新出现的假说。Th1细胞的积聚是导致肉芽肿形成的一系列事件中的关键步骤；此外，一组免疫反应的生物介质定义了可能导致组织损伤的免疫调节网络。人们还认为，Th1/Th2网络的转变以及免疫活性细胞与间充质细胞之间复杂网络的改变可能为肉芽肿性病变周围组织的重塑奠定基础。
