Herold Marco J, Reichardt Holger M
Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.
Crit Rev Immunol. 2013;33(3):183-202. doi: 10.1615/critrevimmunol.2013007415.
Glucocorticoids (GCs) are highly potent anti-inflammatory and immunosuppressive agents. They exert influence on many cell types of the immune system and impact a plethora of processes such as cytokine production, leukocyte differentiation, migration and adhesion, apoptosis induction, and changes in morphology. Those that are most relevant for the modulation of neuroinflammatory diseases, however, are still under debate. In this review, we will elaborate on how GCs impact inflammatory responses in general and revisit the ambivalent role that apoptosis plays in animal models of multiple sclerosis. Furthermore, we will discuss arguments that speak in favor or against an essential function of GC-induced apoptosis in neuroinflammation. We anticipate that a better knowledge of the mechanisms that GCs employ will eventually find its way into clinical practice for the future benefit of afflicted patients.
糖皮质激素(GCs)是强效的抗炎和免疫抑制剂。它们对免疫系统的多种细胞类型产生影响,并影响众多过程,如细胞因子产生、白细胞分化、迁移和黏附、诱导凋亡以及形态变化。然而,那些与神经炎症性疾病调节最为相关的作用仍存在争议。在本综述中,我们将阐述糖皮质激素如何总体上影响炎症反应,并重新审视凋亡在多发性硬化症动物模型中所起的矛盾作用。此外,我们将讨论支持或反对糖皮质激素诱导的凋亡在神经炎症中起关键作用的观点。我们预计,更好地了解糖皮质激素所采用的机制最终将应用于临床实践,以造福患病患者。