Nuclear Receptors Group, Department of Physiology, School of Biology, Barcelona, Spain.
Adv Immunol. 2010;108:1-20. doi: 10.1016/B978-0-12-380995-7.00001-X.
Macrophages play key roles in inflammation. During the onset of the inflammatory process, these phagocytic cells become activated and have destructive effects. Macrophage activation, which involves the induction of more than 400 genes, results in an increased capacity to eliminate bacteria and to regulate many other cells through the release of cytokines and chemokines. However, excessive activation has damaging effects, such as septic shock, which can lead to multiple organ dysfunction syndrome and death. In other situations, persistence of proinflammatory activity results in the development of chronic inflammation, such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. To prevent undesirable effects, several mechanisms have evolved to control the excess of activation, thereby leading to macrophage deactivation and the resolution of inflammation. In this review, we discuss several mechanisms that mediate macrophage deactivation.
巨噬细胞在炎症中发挥关键作用。在炎症过程的开始时，这些吞噬细胞被激活并具有破坏性的影响。巨噬细胞的激活涉及到超过 400 个基因的诱导，导致其增强了消除细菌的能力，并通过细胞因子和趋化因子的释放来调节许多其他细胞。然而，过度激活会产生有害的影响，例如败血症性休克，这可能导致多器官功能障碍综合征和死亡。在其他情况下，促炎活性的持续存在导致慢性炎症的发展，如类风湿关节炎、银屑病和炎症性肠病。为了防止不良影响，已经进化出几种机制来控制过度激活，从而导致巨噬细胞失活和炎症的消退。在这篇综述中，我们讨论了几种介导巨噬细胞失活的机制。
