白癜风发病机制的神经元理论:过去和现在

Mohammed S Al Abadie
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引用次数: 0

摘要

白癜风是一种常见的皮肤病,估计患病率为世界人口的1-2%。它的特征是界限分明的乳白色色斑,有扩大和向周围扩散的趋势。发病机制尚不完全清楚,这一过程导致并最终导致表皮功能黑色素细胞的丧失。人们提出了许多理论和假设,但没有一个能完全解释其发病机制。然而,最近人们认为,这些理论之间的重叠可以提供更好的理解。这包括两个长期存在的理论,即自身免疫和神经元。后者于1959年提出,最初是基于临床观察和研究,包括动物、生理、生化、胚胎、结构和电子显微镜。1994年,通过在白癜风皮肤活动边缘的皮肤中神经肽的变化,特别是神经肽Y (NPY)的变化,出现了将神经元理论与自身免疫机制联系起来的新证据。这篇综述文章强调了过去和现在所有支持白癜风发病机制的神经元理论的证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Neuronal Theory in the Pathogenesis of Vitiligo: Past and Present
Vitiligo is a common skin disorder with an estimated prevalence of 1-2% of the world population. It is characterised by well demarcated milky white patches of depigmentation which have the tendency to enlarge and spread peripherally. The pathogenesis is not fully understood, a process leads and end in the loss of functional melanocytes from the epidermis. There are many proposed theories and hypotheses, none of which can fully explain its pathogenesis. However, lately it is believed that an overlap between some of these theories can present better understanding. This is to include the two long standing theories i.e., the autoimmune and the neuronal. The latter been proposed in 1959, initially based on clinical observations and studies, including animal, physiological, biochemical, embryonic, structural and electron microscopy. In 1994 new evidence emerged linking the neuronal theory to autoimmune mechanisms by demonstration of changes in Neuropeptides in particular Neuropeptide Y (NPY), in the skin at the active edge of vitiligo skin. This review paper highlights all evidence supportive of the neuronal theory in the pathogenesis of vitiligo past and present.
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