Intracellular sensing of microbes and danger signals by the inflammasomes.
Intracellular sensing of microbes and danger signals by the inflammasomes.
复制标题
DOI：
10.1111/j.1600-065x.2011.01050.x
复制
发表时间：
2011-09
影响因子：
8.7
通讯作者：
Latz E
中科院分区：
文献类型：
--
作者：
Horvath GL;Schrum JE;De Nardo CM;Latz E
先天性免疫系统的细胞动员针对入侵微生物的协调免疫应答，并且在组织稳态紊乱之后。这些免疫反应通常导致感染控制和组织修复。然而，夸大或不受控制的免疫应答也可诱导急性或慢性炎性病理，其是许多常见疾病如败血症、关节炎、动脉粥样硬化或阿尔茨海默病的特征。近年来，许多科学家的共同努力已经发现了许多免疫细胞检测感染或组织损伤中出现的外来或改变的自身物质的机制。这些物质刺激信号受体，导致细胞活化和效应机制的诱导。在此，我们综述了炎性小体的作用，炎性小体是形成多分子信号平台并激活炎性半胱氨酸蛋白酶和IL-1β细胞因子的信号分子家族。
The cells of the innate immune system mobilize a coordinated immune response towards invading microbes and after disturbances in tissue homeostasis. These immune responses typically lead to infection control and tissue repair. Exaggerated or uncontrolled immune responses, however, can also induce acute of chronic inflammatory pathologies that are characteristic for many common diseases such as sepsis, arthritis, atherosclerosis or Alzheimer’s disease. In recent years the concerted efforts of many scientists have uncovered numerous mechanisms by which immune cells detect foreign or changed self-substances that appear in infections or during tissue damage. These substances stimulate signaling receptors, which leads to cellular activation and the induction of effector mechanisms. Here, we review the role of inflammasomes, a family of signaling molecules that form multi-molecular signaling platforms and activate inflammatory caspases and IL-1β cytokines.