Department of Cardiovascular and Thoracic Sciences, IRCCS-Fondazione Policlinico Universitario A. Gemelli, Catholic University of the Sacred Heart, Rome, Italy.
Thromb Haemost. 2018 Aug;118(8):1352-1369. doi: 10.1055/s-0038-1666860. Epub 2018 Jul 10.
Over the past few decades, lot of evidences have shown atherosclerosis as a chronic progressive disease with an exquisite inflammatory feature. More recently, the role of innate immune response in the onset and progression of coronary artery disease (CAD) and an adaptive immunity imbalance, mostly involving T cell sub-sets, have been documented. Therefore, like in many other inflammatory and autoimmune disorders, an altered innate-adaptive immunity crosstalk could represent the key of the inflammatory burden leading to atherosclerotic plaque formation and progression and to the breakdown of plaque stability. In this review, we will address the role of inflammasome in innate immunity and in the imbalance of adaptive immunity. We will discuss how this altered immune crosstalk is related to CAD onset and progression. We will also discuss how unravelling the key molecular mechanisms is of paramount importance in the development of therapeutic tools to delay the chronic progression and prevent the acute destabilization of atherosclerotic plaque.
在过去的几十年中，大量证据表明动脉粥样硬化是一种具有精细炎症特征的慢性进行性疾病。最近，先天性免疫反应在冠状动脉疾病 (CAD) 的发生和发展中的作用以及适应性免疫失衡（主要涉及 T 细胞亚群）已被记录在案。因此，与许多其他炎症和自身免疫性疾病一样，先天-适应性免疫相互作用的改变可能代表导致动脉粥样硬化斑块形成和进展以及斑块稳定性破坏的炎症负担的关键。在这篇综述中，我们将讨论炎症小体在先天免疫和适应性免疫失衡中的作用。我们将讨论这种改变的免疫相互作用与 CAD 发病和进展的关系。我们还将讨论阐明关键分子机制在开发治疗工具以延缓慢性进展和预防动脉粥样硬化斑块的急性不稳定方面的重要性。
