Brea David, Sobrino Tomás, Ramos-Cabrer Pedro, Castillo José
Clinical Neuroscience Research Laboratory, Department of Neurology, Hospital Clínico Universitario de Santiago de Compostela, University of Santiago de Compostela, Santiago de Compostela, Spain.
Cerebrovasc Dis. 2009;27 Suppl 1:48-64. doi: 10.1159/000200441. Epub 2009 Apr 3.
Neuronal death produced by cerebral ischemia activates innate immunity by Toll-like receptors and triggers inflammatory response. This response is necessary to remove cell debris and to start regenerative process. However, inflammatory response could exacerbate cerebral damage and it is involved in secondary brain damage. Therefore, organisms have developed different mechanisms to regulate inflammatory response. An accurate balance between inflammation and anti-inflammation is necessary to assure the removal of cell debris and to avoid secondary cell damage. New therapeutic targets could be designed to obtain a correct modulation of the immune system and to reduce cerebral brain damage after cerebral ischemia. In this paper, we review the function of the immune system in cerebral ischemia, particularly inflammation and immunomodulation.
脑缺血导致的神经元死亡通过Toll样受体激活先天免疫并引发炎症反应。这种反应对于清除细胞碎片和启动再生过程是必要的。然而，炎症反应可能会加剧脑损伤，并且它参与继发性脑损伤。因此，生物体已经发展出不同的机制来调节炎症反应。炎症与抗炎之间的精确平衡对于确保细胞碎片的清除和避免继发性细胞损伤是必要的。可以设计新的治疗靶点来实现对免疫系统的正确调节，并减少脑缺血后的脑损伤。在本文中，我们综述了免疫系统在脑缺血中的功能，特别是炎症和免疫调节。
