Laboratorio de Neuroinflamación, Unidad de Neurología Experimental, Hospital Nacional de Parapléjicos-SESCAM, Finca La Peraleda, Toledo, Spain.
J Neurochem. 2010 Sep 1;114(5):1277-90. doi: 10.1111/j.1471-4159.2010.06849.x. Epub 2010 Jun 8.
Neuroimmune networks and the brain endocannabinoid system contribute to the maintenance of neurogenesis. Cytokines and chemokines are important neuroinflammatory mediators that are involved in the pathological processes resulting from brain trauma, ischemia and chronic neurodegenerative diseases. However, they are also involved in brain repair and recovery. Compelling evidence obtained, in vivo and in vitro, establish a dynamic interplay between the endocannabinoid system, the immune system and neural stem/progenitor cells (NSC) in order to promote brain self-repair. Cross-talk between inflammatory mediators and NSC might have important consequences for neural development and brain repair. In addition, brain immune cells (microglia) support NSC renewal, migration and lineage specification. The proliferation and differentiation of multipotent NSC must be precisely controlled during the development of the CNS, as well as for adult brain repair. Although signalling through neuroimmune networks has been implicated in many aspects of neural development, how it affects NSC remains unclear. However, recent findings have clearly demonstrated that there is bi-directional cross-talk between NSC, and the neuroimmune network to control the signals involved in self-renewal and differentiation of NSC. Specifically, there is evidence emerging that neuroimmune interactions control the generation of new functional neurones from adult NSC. Here, we review the evidence that neuroimmune networks contribute to neurogenesis, focusing on the regulatory mechanisms that favour the immune system (immune cells and immune molecules) as a novel element in the coordination of the self-renewal, migration and differentiation of NSC in the CNS. In conjunction, these data suggest a novel mode of action for the immune system in neurogenesis that may be of therapeutic interest in the emerging field of brain repair.
神经免疫网络和大脑内源性大麻素系统有助于维持神经发生。细胞因子和趋化因子是重要的神经炎症介质，参与脑创伤、缺血和慢性神经退行性疾病引起的病理过程。然而，它们也参与了大脑的修复和恢复。体内和体外获得的强有力证据表明，内源性大麻素系统、免疫系统和神经干细胞/祖细胞（NSC）之间存在动态相互作用，以促进大脑自我修复。炎症介质和 NSC 之间的串扰可能对神经发育和大脑修复有重要影响。此外，大脑免疫细胞（小胶质细胞）支持 NSC 的更新、迁移和谱系特化。多能 NSC 的增殖和分化必须在中枢神经系统发育过程中以及成人大脑修复过程中得到精确控制。尽管神经免疫网络的信号转导已被涉及到许多方面的神经发育，但它如何影响 NSC 尚不清楚。然而，最近的发现清楚地表明，NSC 与神经免疫网络之间存在双向串扰，以控制涉及 NSC 自我更新和分化的信号。具体来说，有证据表明，神经免疫相互作用控制着成年 NSC 产生新的功能性神经元。在这里，我们综述了神经免疫网络促进神经发生的证据，重点讨论了有利于免疫系统的调节机制（免疫细胞和免疫分子）作为协调中枢神经系统 NSC 自我更新、迁移和分化的新因素。这些数据共同表明，免疫系统在神经发生中的作用具有新的模式，这可能在新兴的大脑修复领域具有治疗意义。
