Autonomic innervation and regulation of the immune system (1987-2007)

Autonomic innervation and regulation of the immune system (1987-2007)
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DOI:
10.1016/j.bbi.2007.03.008
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发表时间:
2007-08-01
影响因子:
15.1
通讯作者:
Sanders, Virginia M.
Sanders, Virginia M.
中科院分区:
医学1区
文献类型:
--
作者:
Nance, Dwight M.;Sanders, Virginia M.

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自1987年以来,仅进行了少数神经解剖学研究以确定免疫系统神经支配的起源。这些研究表明,所有初级和次级免疫器官都接受来自交感神经节后神经元的大量交感神经支配。胸腺和脾脏都没有任何感觉神经支配;然而,有证据表明淋巴结和骨髓可能由位于背根神经节的感觉神经元支配。没有神经解剖学证据表明任何免疫器官存在副交感神经或迷走神经供应。因此,免疫功能神经调节的主要途径是由交感神经系统(SNS)及其主要神经递质去甲肾上腺素(NE)提供的。交感神经系统的激活主要抑制与固有免疫系统相关细胞的活性,而它要么增强要么抑制与获得性/适应性免疫系统相关细胞的活性。固有免疫细胞表达α和β - 肾上腺素能受体亚型,而T和B淋巴细胞仅表达β2亚型的肾上腺素能受体,但小鼠Th2细胞除外,它不表达任何亚型。通过这些肾上腺素能受体,NE能够通过引发细胞活性水平的变化来调节免疫细胞活性水平,这通常涉及细胞因子和抗体基因表达水平的变化。(C)2007爱思唯尔公司。保留所有权利。
Since 1987, only a few neuroanatomical studies have been conducted to identify the origin of innervation for the immune system. These studies demonstrated that all primary and secondary immune organs receive a substantial sympathetic innervation from sympathetic postganglionic neurons. Neither the thymus nor spleen receive any sensory neural innervation; however, there is evidence that lymph nodes and bone marrow may be innervated by sensory neurons located in dorsal root ganglia. There is no neuroanatomical evidence for a parasympathetic or vagal nerve supply to any immune organ. Thus, the primary pathway for the neural regulation of immune function is provided by the sympathetic nervous system (SNS) and its main neurotransmitter, norepinephrine (NE). Activation of the SNS primarily inhibits the activity of cells associated with the innate immune system, while it either enhances or inhibits the activity of cells associated with the acquired/adaptive immune system. Innate immune cells express both alpha and beta-adrenergic receptor subtypes, while T and B lymphocytes express adrenergic receptors of the beta2 subtype exclusively, except for murine Th2 cells that lack expression of any subtype. Via these adrenergic receptors, NE is able to regulate the level of immune cell activity by initiating a change in the level of cellular activity, which often involves a change in the level of gene expression for cytokines and antibodies. (C) 2007 Elsevier Inc. All rights reserved.