a Department of Medicine , The Ohio State University Wexner Medical Center , Columbus , OH , USA.
Expert Opin Biol Ther. 2018 Apr;18(4):399-407. doi: 10.1080/14712598.2018.1427727. Epub 2018 Jan 17.
Sarcoidosis is a chronic granulomatous inflammatory disease that commonly causes lung disease, but can affect other vital organs and tissues. The cause of sarcoidosis is unknown, and current therapies are commonly limited by lack of efficacy, adverse side effects, and excessive cost.
The manuscript will provide a review of current concepts relating to the pathogenesis of sarcoidosis, and how these disease mechanisms may be leveraged to develop more effective treatments for sarcoidosis. It provides only a brief summary of currently accepted therapy, while focusing more extensively on potential novel therapies.
Current sarcoidosis therapeutic agents primarily target the M1 or pro-inflammatory pathways. Agents that prevent M2 polarization, a regulatory phenotype favoring fibrosis, are attractive treatment alternatives that could potentially prevent fibrosis and associated life threatening complications. Effective treatment of sarcoidosis potentially requires simultaneous modulation both M1/M2 polarization instead of suppressing one pathway over the other to restore immune competent and inactive (M0) macrophages.
结节病是一种慢性肉芽肿性炎症性疾病，通常会导致肺部疾病，但也可能影响其他重要器官和组织。结节病的病因尚不清楚，目前的治疗方法通常因疗效不佳、不良反应和费用过高而受到限制。
本文将回顾与结节病发病机制相关的当前概念，以及如何利用这些疾病机制开发更有效的结节病治疗方法。它仅简要总结了目前公认的治疗方法，而更广泛地侧重于潜在的新型治疗方法。
目前的结节病治疗药物主要针对 M1 或促炎途径。预防 M2 极化的药物是一种有吸引力的治疗选择，M2 极化是一种有利于纤维化的调节表型，可能潜在地预防纤维化和相关的危及生命的并发症。结节病的有效治疗可能需要同时调节 M1/M2 极化，而不是抑制一条途径而不是另一条途径，以恢复免疫功能正常和无活性（M0）巨噬细胞。
