Chen Edward S, Moller David R
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA.
Clin Chest Med. 2008 Sep;29(3):365-77, vii. doi: 10.1016/j.ccm.2008.03.011.
Research over the past decade has advanced our understanding of the pathogenesis of sarcoidosis and provided new insights into potential causes of this disease. It is important to remember that any etiologic agent of sarcoidosis must be capable of causing the pathologic hallmark of systemic noncaseating granulomas and the heterogeneous clinical features of sarcoidosis. In addition, etiologic agents must be compatible with immunologic features, including polarized T-helper 1 cytokine profiles and oligoclonal T cell expansions consistent with antigen driven processes. Yet, even with studies conducted in this disease, there remains a lack of consensus on the etiology of sarcoidosis. This challenge is likely to be overcome only with additional research that incorporates clinical, genetic, immunologic, environmental, and microbiologic profiles in groups of patients, supplemented with testing of candidate pathogenic agents in experimental models that recapitulate critical features of this disease.
过去十年的研究增进了我们对结节病发病机制的理解,并为该疾病的潜在病因提供了新的见解。必须记住,任何结节病的病因都必须能够引发系统性非干酪样肉芽肿的病理特征以及结节病的异质性临床特征。此外,病因必须与免疫特征相符,包括极化的辅助性T细胞1细胞因子谱以及与抗原驱动过程一致的寡克隆T细胞扩增。然而,即便针对该疾病开展了诸多研究,对于结节病的病因仍未达成共识。只有通过更多的研究才有可能克服这一挑战,这些研究需纳入患者群体的临床、遗传、免疫、环境和微生物学特征,并辅以在重现该疾病关键特征的实验模型中对候选病原体进行检测。