Gerke Alicia K, Hunninghake Gary
Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa College of Medicine, 200 Hawkins Drive, Iowa City, IA 52242, USA.
Clin Chest Med. 2008 Sep;29(3):379-90, vii. doi: 10.1016/j.ccm.2008.03.014.
Sarcoidosis continues to be a disease of research interest because of its complicated immune mechanisms and elusive etiology. So far, it has been established that granulomatous inflammation in sarcoidosis is predominantly a T-helper 1 immune response mediated by a complex network of lymphocytes, macrophages, and cytokines. The cause of progression to a chronic and potentially fibrotic form is unclear but may involve loss of apoptotic mechanisms, loss of regulatory response, or a persistent antigen that cannot be cleared. Recent genomic and proteomic technology has emphasized the importance of host susceptibility and gene-environment interaction in the expression of the disease.
结节病因其复杂的免疫机制和难以捉摸的病因，一直是研究热点。目前已经明确，结节病中的肉芽肿性炎症主要是由淋巴细胞、巨噬细胞和细胞因子组成的复杂网络介导的辅助性T细胞1免疫反应。进展为慢性且可能纤维化形式的原因尚不清楚，但可能涉及凋亡机制丧失、调节反应缺失或存在无法清除的持续抗原。最近的基因组和蛋白质组技术强调了宿主易感性以及基因-环境相互作用在该疾病表达中的重要性。
