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单细胞和空间测序定义了质细胞和纤维细胞放大牛皮炎炎症反应的过程

Feiyang Ma^1,2,3, Olesya Plazyo², Allison C Billi²

¹Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109, USA.

Nature communications

|June 12, 2023

概括

牛皮的炎症涉及IL-36信号和特定的纤维细胞. 这些SFRP2+纤维细胞通过与髓状细胞和树突细胞相互作用来放大免疫反应,从而导致皮肤炎症.

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:

牛皮是一种常见的慢性炎症性皮肤病,免疫病原生成的理解不佳.
现有研究尚未完全阐明导致牛皮炎的复杂细胞相互作用.

研究的目的:

为了研究背后的细胞和分子机制牛皮免疫病原发生.
识别导致牛皮皮肤炎症的新型细胞参与者和相互作用.

主要方法:

利用单细胞和空间RNA测序来分析牛皮皮肤组织.
研究了介素-36 (IL-36) 和纤维细胞亚群在炎症中的作用.
在牛皮微环境中,在不同细胞类型之间映射了连接体-受体相互作用.

主要成果:

证明IL-36依赖于IL-17A和TNF反应的放大,独立于中性粒细胞蛋白酶.
鉴定出SFRP2+纤维细胞的一个子集在牛皮中过渡到促炎状态.
通过特定的化学因子和受体 (CCL13,CCL19,CXCL12,CCR2,CCR7,LAMP3,CXCR4) 揭示了一种涉及SFRP2+纤维细胞,髓质细胞,树突细胞,CD8+Tc17细胞和角质细胞的通信网络.
显示的SFRP2+纤维细胞通过cathepsin S激活 keratinocytes中的IL-36G,进一步放大炎症.

结论:

牛皮病的发病包括免疫细胞和炎症性纤维细胞的特定子集之间的复杂相互作用.
通过广泛的细胞通信和细胞因子激活,SFRP2+纤维细胞在放大牛皮炎炎症方面发挥着关键作用.
这些发现通过突出炎症性纤维细胞作为关键细胞参与者来扩大对牛皮病变的理解.

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