Immunology Research Centre, Inflammation Research Group, School of Biochemistry and Immunology, Trinity College Dublin, Ireland.
Trends Mol Med. 2011 May;17(5):276-82. doi: 10.1016/j.molmed.2011.01.005. Epub 2011 Mar 2.
The pathogenesis of type 2 diabetes, Alzheimer's disease and amyotrophic lateral sclerosis continues to be debated. Recently, the inflammasome protein complex has been shown to be a key regulator of IL-1β, a cytokine implicated in each of these diseases. In all three cases, it is now apparent that unique protein aggregates caused by inappropriate oligomerization or misfolding are sensed by the inflammasome, providing a unifying mechanism for this IL-1β production. What evolved as an innate defense against infection-related particles, therefore, now seems to be a driving force for inflammation in these diseases. This review discusses the basic research behind these findings and the potential for new therapeutic interventions this affords.
2 型糖尿病、阿尔茨海默病和肌萎缩侧索硬化症的发病机制仍存在争议。最近，炎症小体蛋白复合物已被证明是白细胞介素-1β（IL-1β）的关键调节剂，而白细胞介素-1β与这三种疾病都有关联。目前已十分清楚，在这三种情况下，由不适当的寡聚化或错误折叠引起的独特蛋白质聚集体被炎症小体识别，为这种白细胞介素-1β的产生提供了一个统一的机制。因此，作为一种针对与感染相关的颗粒的先天防御机制，现在似乎成了这些疾病中炎症的驱动力。本综述讨论了这些发现背后的基础研究以及为此提供的新的治疗干预的潜力。
