Hori T, Katafuchi T, Take S, Shimizu N, Niijima A
Department of Physiology, Kyushu University Faculty of Medicine, Fukuoka, Japan.
Neuroimmunomodulation. 1995 Jul-Aug;2(4):203-15. doi: 10.1159/000097198.
Much evidence from various fields has revealed multiple channels of communication between the brain and the immune system. Among the routes of signal transmission, this review focuses on the roles and mechanisms of neural communication between the two systems. As for the centrifugal neural pathway by which the brain modulates immunity, there are various requirements for the noradrenergic sympathetic innervation of the primary and secondary lymphoid organs. In addition to the presence of beta- and alpha-adrenergic receptors on different types of immunocompetent cells, histological studies have demonstrated direct contact between tyrosine-hydroxylase-positive nerve terminals and lymphocytes in the spleen and thymus. The exposure of lymphocytes and macrophages to adrenergic agonists in vitro modulates their functions. A surgical or chemical sympathectomy is known to alter the immune responses in rodents. Recent data from the rat show that stress-induced immunosuppression is only slightly affected, if at all, by hypophysectomy or adrenalectomy, whereas it is largely dependent on sympathetic innervation. The splenic sympathetic nerve alters the firing rate by an ablation or stimulation of the hypothalamus, the administration of cytokines or neuropeptides, and an exposure to stress. Furthermore, such procedures provoke the increase in the release of noradrenaline in the rat spleen as assessed by in vivo microdialysis. The altered activities of the splenic sympathetic nerves mentioned above have been found to be causally related to the alteration in immunological responses including natural killer cytotoxicity. The splenic sympathetic nerve may thus constitute a communication channel that mediates central modulation of peripheral cellular immunity. Although the roles and mechanisms of parasympathetic control of lymphoid organs still remain obscure, recent data suggest that the thymic vagal efferent nerve may be involved in central modulation of immunity. Finally, electrophysiological studies have shown that hepatic vagal afferents may be one of the pathways through which blood-borne cytokines signal the brain.
来自各个领域的大量证据揭示了大脑与免疫系统之间的多种通讯渠道。在信号传递途径中，本综述重点关注这两个系统之间神经通讯的作用和机制。至于大脑调节免疫的离心神经通路，初级和次级淋巴器官的去甲肾上腺素能交感神经支配存在各种要求。除了不同类型的免疫活性细胞上存在β-和α-肾上腺素能受体外，组织学研究还表明酪氨酸羟化酶阳性神经末梢与脾脏和胸腺中的淋巴细胞有直接接触。体外将淋巴细胞和巨噬细胞暴露于肾上腺素能激动剂可调节它们的功能。已知手术或化学交感神经切除术会改变啮齿动物的免疫反应。来自大鼠的最新数据表明，应激诱导的免疫抑制即使受到垂体切除术或肾上腺切除术的影响也很小，而它很大程度上依赖于交感神经支配。脾脏交感神经通过切除或刺激下丘脑、给予细胞因子或神经肽以及暴露于应激来改变放电频率。此外，通过体内微透析评估，这些程序会促使大鼠脾脏中去甲肾上腺素的释放增加。已发现上述脾脏交感神经活动的改变与包括自然杀伤细胞细胞毒性在内的免疫反应改变存在因果关系。因此，脾脏交感神经可能构成一个介导外周细胞免疫中枢调节的通讯通道。尽管副交感神经对淋巴器官的控制作用和机制仍不清楚，但最近的数据表明胸腺迷走传出神经可能参与免疫的中枢调节。最后，电生理研究表明肝迷走传入神经可能是血源性细胞因子向大脑发出信号的途径之一。
