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在牛皮中,S100A8和S100A9介导的角质细胞通过TLR4/NF-κ B影响T淋巴细胞免疫失衡

Yali He¹, Jianxiao Xing², Junqin Li³

¹Ninth Clinical College of Medicine, Shanxi Medical University, Taiyuan, China; Department of Dermatology, the Second People's Hospital of Taiyuan City, Taiyuan, China; Department of Dermatology, Taiyuan Central Hospital, Shanxi Medical University, Taiyuan, China; Key Laboratory of Stem Cells for Immunologic Skin Diseases, Taiyuan Central Hospital, Taiyuan, China.

Acta histochemica

|November 18, 2025

概括

S100A8和S100A9蛋白在牛皮中高度表达,并通过激活TLR4/NF-κB通路来促进皮肤炎症. 抑制这些蛋白质可以减少小鼠模型中的牛皮症状和炎症.

科学领域:

皮肤病学皮肤病学
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

牛皮是一种慢性炎症性皮肤疾病.
S100A8和S100A9是已知的炎症警示蛋白,涉及慢性炎症.
S100A8和S100A9在牛皮病原体中的特定作用尚未完全理解.

研究的目的:

研究S100A8和S100A9在牛皮的作用和潜在机制.
阐明S100A8和S100A9在牛皮炎和角质细胞增殖中的作用.

主要方法:

评估了在细胞因子治疗细胞中的S100A8和S100A9表达,以及一个因伊米基莫德 (IMQ) 诱导的牛皮小鼠模型.
在正常人表皮皮质角质细胞 (NHEK) 中击败S100A8和S100A9,并与T细胞共培养它们.
研究了托尔类受体4 (TLR4) /NF-κB信号通路,并在IMQ小鼠模型中使用了抑制剂帕基尼莫德.

主要成果:

在牛皮模型中,S100A8和S100A9的表达很高,并刺激了NHEK细胞的增殖.
通过TLR4/NF-κB激活,S100A8和S100A9促进了T细胞通过TLR4/NF-κB激活产生促炎性细胞因子.
在小鼠中,Paquinimod治疗减少了牛皮皮炎,炎症和TLR4/NF-κB表达.

结论:

通过激活TLR4/NF-κB信号传递,S100A8和S100A9通过激活TLR4/NF-κB信号传递,促进了牛皮病的发生.
这些蛋白质促进与牛皮相关的皮肤炎症.
S100A8和S100A9代表了牛皮的潜在治疗点.

关键词:

炎症炎症是一种炎症.牛皮是一种病.在S100A8A8中使用.在S100A9A9中使用.通过TLR4/NF-κ B途径.

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