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免疫调节蛋白在接口皮肤病中的免疫组织化学表达

Sarah Grace McAlpine¹, Donna Culton^1,2, Michael Duplisea¹

¹University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.

Journal of cutaneous pathology

|October 25, 2024

概括

像PD-L1和LAG-3这样的免疫检查点蛋白在各种皮肤疾病中升高,这表明先天性免疫因素与T细胞反应一起有助于介面皮肤炎.

科学领域:

皮肤病学皮肤病学
免疫学免疫学免疫学
病理生物学病理生物学

背景情况:

免疫疗法引起的皮肤免疫相关不良事件强调了免疫检查点的作用.
在未接受免疫治疗的患者中,状界面皮肤炎 (LID) 的病理生物学尚未完全理解.
现有的理论暗示细胞介导免疫和CD8+T细胞在质细胞亡中.

研究的目的:

在五种类型的状界面皮肤病中研究先天性和适应性免疫标志物.
使用免疫组织化学比较PD-L1,STING,IL-36马,CD8,PD-1和LAG-3的表达.
探索先天性免疫因子对LID病原性的贡献.

主要方法:

免疫组织化学 (IHC) 染色是在口腔平斑 (LP),皮肤LP,慢性皮肤红斑狼 (CLE),多形红斑 (EM) 和有毒表皮解 (TEN) 患者的皮肤活检样本上进行的.
半定量评估了PD-L1,STING,IL-36马,CD8,PD-1和LAG-3的表达水平.
染色模式与正常人皮肤对照进行了比较.

主要成果:

在所有评估的界面皮肤病中观察到PD-L1 (角质细胞) 和LAG-3 (淋巴细胞) 的表达增加.
在大多数标本中,SING表达在角质细胞中升高.
在口服和皮肤LP中,IL-36马表达更为突出,而PD-1在口服LP,皮肤LP和CLE中升高.

结论:

这些发现表明,先天性免疫因子,包括STING和IL-36 gamma,在接口皮肤病变的病理生物学中起作用.
增加PD-L1和LAG-3表达表明免疫检查点通路的参与.
LID的发病可能涉及适应性细胞介导免疫和先天性免疫机制.

关键词:

适应性免疫是一种适应性免疫.自发炎性疾病是自发炎性疾病.免疫调节疗法是一种免疫调节疗法.这是先天免疫力.接口皮肤病的接口皮肤病.

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