Immunopathogenesis of skin injury in systemic lupus erythematosus.
Immunopathogenesis of skin injury in systemic lupus erythematosus.
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系统性红斑狼疮皮肤损伤的免疫发病机制。
DOI：
10.1097/bor.0000000000000770
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发表时间：
2021-03-01
影响因子：
5.1
通讯作者：
Kahlenberg JM
中科院分区：
文献类型：
--
作者：
Hile GA;Kahlenberg JM
皮肤损伤是系统性红斑狼疮最常见的临床表现，并且毁容、难以治疗且不完全了解。我们提供了一个概述最近发表的文章，涵盖了SLE皮肤损伤的免疫发病机制的SLE皮肤具有固有的易感性细胞凋亡，其病因可能是多因素的。慢性IFN过表达导致屏障破坏、炎性细胞浸润、细胞因子产生和自身抗原释放以及导致皮肤损伤的自身抗体产生。紫外线是最重要的CLE触发器，并放大这一过程，导致皮肤炎症和潜在的全身性疾病爆发。CLE中皮肤损伤的发病机制是复杂的，但最近的研究强调了驱动失调的表皮细胞死亡的机制的重要性，这些机制可能受到遗传风险因素、环境触发因素（UV光）以及细胞毒性细胞和细胞信号传导的影响。
Skin injury is the most common clinical manifestation of SLE and is disfiguring, difficult to treat, and incompletely understood. We provide an overview of recently published articles covering the immunopathogenesis of skin injury in SLE Skin of SLE has an inherent susceptibility to apoptosis, the etiology of which may be multifactorial. Chronic IFN overexpression leads to barrier disruption, infiltration of inflammatory cells, cytokine production and release of autoantigens and autoantibody production that result in skin injury. Ultraviolet light is the most important CLE trigger and amplifies this process leading to skin inflammation and potentially systemic disease flares. The pathogenesis of skin injury in CLE is complex but recent studies highlight the importance of mechanisms driving dysregulated epidermal cell death likely influenced by genetic risk factors, environmental triggers (UV light), and cytotoxic cells and cellular signaling.