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皮肤树突状细胞的神经内分泌调节

Neuroendocrine regulation of skin dendritic cells.

作者信息

Seiffert Kristina, Granstein Richard D

机构信息

Division of Dermatology and Cutaneous Sciences, Michigan State University, East Lansing, Michigan, USA.

出版信息

Ann N Y Acad Sci. 2006 Nov;1088:195-206. doi: 10.1196/annals.1366.011.

DOI:10.1196/annals.1366.011
PMID:17192566
Abstract

It has long been postulated that stress can affect certain skin conditions, and there is increasing experimental evidence that the neuroendocrine system can directly participate in cutaneous inflammation. Neurohormones, such as glucocorticoids and catecholamines, can reach the skin through the bloodstream after activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, respectively. Multiple neuropeptides, among them calcitonin gene-related peptide, alpha-melanocyte stimulating hormone, pituitary adenylate cyclase-activating peptide, substance P, vasoactive intestinal peptide, and norepinephrine, may be released by cutaneous nerves or resident and infiltrating cells within the skin. Systemic neuromediators and cutaneous nerves can influence a number of target cells within the skin, among them Langerhans cells. Most of the experimental evidence to date indicates a suppressive effect of the neurohormones and neuropeptides on Langerhans cell function and cutaneous inflammation, but it has become evident lately that the timing of exposure to a stimulus is critical to the outcome of the immune response. Thus, administration of a stress hormone or exposure to a stressor before the dendritic cell (DC) encounters an antigen (Ag) may diminish the immune response toward that Ag, while a stressor may enhance immune function when acting on a maturing DC or before reexposure to the Ag. The neuroendocrine regulation of skin DCs is a complex system allowing for a quick adaptation to various stressors. Such a system, originally evolved to defend the organism against invading pathogens and maintain homeostasis, may under certain conditions become unbalanced and ultimately exacerbate cutaneous inflammation.

摘要

长期以来,人们一直推测压力会影响某些皮肤状况,并且越来越多的实验证据表明神经内分泌系统可直接参与皮肤炎症。神经激素,如糖皮质激素和儿茶酚胺,可分别在下丘脑 - 垂体 - 肾上腺轴和交感神经系统激活后通过血液循环到达皮肤。多种神经肽,包括降钙素基因相关肽、α - 黑素细胞刺激素、垂体腺苷酸环化酶激活肽、P物质、血管活性肠肽和去甲肾上腺素,可能由皮肤神经或皮肤内的驻留细胞和浸润细胞释放。全身神经介质和皮肤神经可影响皮肤内的多种靶细胞,其中包括朗格汉斯细胞。迄今为止,大多数实验证据表明神经激素和神经肽对朗格汉斯细胞功能和皮肤炎症具有抑制作用,但最近已明显看出,接触刺激的时间对免疫反应的结果至关重要。因此,在树突状细胞(DC)遇到抗原(Ag)之前给予应激激素或暴露于应激源可能会减弱对该Ag的免疫反应,而应激源在作用于成熟的DC时或再次暴露于Ag之前可能会增强免疫功能。皮肤DC的神经内分泌调节是一个复杂的系统,可快速适应各种应激源。这样一个最初进化来保护机体抵御入侵病原体并维持体内平衡的系统,在某些情况下可能会失衡并最终加剧皮肤炎症。

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