银屑病
脂质代谢
免疫系统
血脂异常
伊米奎莫德
自噬
朗格汉斯细胞
白癜风
免疫学
医学
生物
内分泌学
糖尿病
生物化学
细胞凋亡
作者
Xilin Zhang,Xiaorui Li,Yuanyuan Wang,Youdong Chen,Yijun Hu,Chunyuan Guo,Zengyang Yu,Peng Xu,Yangfeng Ding,Qing‐Sheng Mi,Jihuai Wu,Jun Gu,Yujun Shi
出处
期刊:JCI insight
[American Society for Clinical Investigation]
日期:2022-07-08
卷期号:7 (13)
被引量:9
标识
DOI:10.1172/jci.insight.150223
摘要
Psoriasis is a chronic, inflammatory skin disease, frequently associated with dyslipidemia. Lipid disturbance in psoriasis affects both circulatory system and cutaneous tissue. Epidermal Langerhans cells (LCs) are tissue-resident DCs that maintain skin immune surveillance and mediate various cutaneous disorders, including psoriasis. However, the role of LCs in psoriasis development and their lipid metabolic alternation remains unclear. Here, we demonstrate that epidermal LCs of psoriasis patients enlarge with longer dendrites and possess elevated IL-23p19 mRNA and a higher level of neutral lipids when compared with normal LCs of healthy individuals. Accordantly, epidermal LCs from imiquimod-induced psoriasis-like dermatitis in mice display overmaturation, enhanced phagocytosis, and excessive secretion of IL-23. Remarkably, these altered immune properties in lesional LCs are tightly correlated with elevated neutral lipid levels. Moreover, the increased lipid content of psoriatic LCs might result from impaired autophagy of lipids. Bulk RNA-Seq analysis identifies dysregulated genes involved in lipid metabolism, autophagy, and immunofunctions in murine LCs. Overall, our data suggest that dysregulated lipid metabolism influences LC immunofunction, which contributes to the development of psoriasis, and therapeutic manipulation of this metabolic process might provide an effective measurement for psoriasis.
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