Immunometabolism in the pathogenesis of vitiligo.

Immunometabolism in the pathogenesis of vitiligo.
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白癜风发病机制中的免疫代谢。

DOI:
10.3389/fimmu.2022.1055958
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发表时间:
2022
影响因子:
7.3
通讯作者:
Sun, Yonghu
Sun, Yonghu
中科院分区:
医学2区
文献类型:
--
作者:
Lyu, Chen;Sun, Yonghu

文献摘要

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相似文献

白癜风是一种常见的色素脱失性皮肤病,其特征是黑素细胞的选择性丢失。自身免疫、遗传、环境和生化病因学已被提出在白癜风发病机制中。然而,白癜风发展和进展的确切分子机制尚不清楚,特别是免疫代谢。零星的研究表明,线粒体功能障碍,氧化应激增强,以及其他代谢途径的特定缺陷可以促进白癜风先天性和适应性免疫反应的失调。这些异常似乎是由随机事件调制的遗传和表观遗传因素驱动的。此外,糖脂代谢异常也与白癜风有关。特定的皮肤细胞群也参与代谢途径失调的关键作用,包括黑素细胞、角质形成细胞和组织驻留记忆T细胞在白癜风发病机制中的作用。基于免疫代谢的异常也提出了新的治疗方法。本文综述了白癜风发病机制中的免疫代谢重编程和新的治疗选择。
Vitiligo is a common depigmenting skin disorder characterized by the selective loss of melanocytes. Autoimmunity, genetic, environmental, and biochemical etiology have been proposed in vitiligo pathogenesis. However, the exact molecular mechanisms of vitiligo development and progression are unclear, particularly for immunometabolism. Sporadic studies have suggested mitochondrial dysfunction, enhanced oxidative stress, and specific defects in other metabolic pathways can promote dysregulation of innate and adaptive immune responses in vitiligo. These abnormalities appear to be driven by genetic and epigenetic factors modulated by stochastic events. In addition, glucose and lipid abnormalities in metabolism have been associated with vitiligo. Specific skin cell populations are also involved in the critical role of dysregulation of metabolic pathways, including melanocytes, keratinocytes, and tissue-resident memory T cells in vitiligo pathogenesis. Novel therapeutic treatments are also raised based on the abnormalities of immunometabolism. This review summarizes the current knowledge on immunometabolism reprogramming in the pathogenesis of vitiligo and novel treatment options.
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